Journal Description
Biomedicines
Biomedicines
is an international, peer-reviewed, open access journal on biomedicines published monthly online by MDPI. The Society for Regenerative Medicine (Russian Federation) (RPO) is affiliated with Biomedicines and its members receive discounts on the article processing charges.
- Open Access— free for readers, with article processing charges (APC) paid by authors or their institutions.
- High Visibility: indexed within Scopus, SCIE (Web of Science), PubMed, PMC, CAPlus / SciFinder, and other databases.
- Journal Rank: JCR - Q1 (Pharmacology & Pharmacy) / CiteScore - Q2 (Medicine (miscellaneous))
- Rapid Publication: manuscripts are peer-reviewed and a first decision is provided to authors approximately 15.4 days after submission; acceptance to publication is undertaken in 2.9 days (median values for papers published in this journal in the second half of 2023).
- Recognition of Reviewers: reviewers who provide timely, thorough peer-review reports receive vouchers entitling them to a discount on the APC of their next publication in any MDPI journal, in appreciation of the work done.
- Companion journals for Biomedicines include: IJTM, BioMed, Anesthesia Research and Emergency Care and Medicine.
Impact Factor:
4.7 (2022);
5-Year Impact Factor:
4.9 (2022)
Latest Articles
Seroprevalence and Associated Risk Factors of Toxoplasma gondii in Patients Diagnosed with Schizophrenia: A Case–Control Cross Sectional Study
Biomedicines 2024, 12(5), 998; https://doi.org/10.3390/biomedicines12050998 (registering DOI) - 01 May 2024
Abstract
The protozoan parasite, Toxoplasma gondii, has been linked to several psychiatric disorders, including schizophrenia. The aim of this study was to assess the prevalence of T. gondii IgG antibodies and risk factors associated with seroprevalence in patients diagnosed with schizophrenia. This seroepidemiological
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The protozoan parasite, Toxoplasma gondii, has been linked to several psychiatric disorders, including schizophrenia. The aim of this study was to assess the prevalence of T. gondii IgG antibodies and risk factors associated with seroprevalence in patients diagnosed with schizophrenia. This seroepidemiological study assessed 196 participants, divided into two groups. The study group consisted of 98 schizophrenic patients and was matched with 98 healthy blood donors. A questionnaire was used to gather information regarding potential risk factors associated with T. gondii seroprevalence. Results revealed a higher seroprevalence of T. gondii IgG antibodies in schizophrenic patients (69.39%, 68/98) when compared to healthy controls (51.02%, 50/98) (OR: 2.18; 95% CI: 1.21–3.9; p = 0.01). Patients with schizophrenia who consumed raw or undercooked meat (80.65%, 25/31) (OR: 3.75; 95% CI: 1.25–11.21, p = 0.02) and those with a lower educational level (77.59%, 45/58) (OR: 3.5; 95% CI: 1.59–7.54, p = 0.002) presented increased T. gondii seropositivity rates versus their control counterparts. Our findings indicate a high T. gondii IgG seroprevalence in patients diagnosed with schizophrenia compared to healthy blood donors. Factors associated with T. gondii seroprevalence were consumption of raw or uncooked meat and a lower educational attainment. This study provided the first data regarding the potential risk factors for toxoplasmosis in Romanian patients diagnosed with schizophrenia and may serve as a foundation for future research and the development of preventive strategies.
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(This article belongs to the Special Issue Pathogenesis, Prophylaxis and Treatment of Infectious Diseases)
Open AccessArticle
Influence of the Tissue Collection Procedure on the Adipogenic Differentiation of Human Stem Cells: Ischemic versus Well-Vascularized Adipose Tissue
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Pallabi Pal, Abelardo Medina, Sheetal Chowdhury, Courtney A. Cates, Ratna Bollavarapu, Jon M. Person, Benjamin McIntyre, Joshua S. Speed and Amol V. Janorkar
Biomedicines 2024, 12(5), 997; https://doi.org/10.3390/biomedicines12050997 (registering DOI) - 01 May 2024
Abstract
Clinical and basic science applications using adipose-derived stem cells (ADSCs) are gaining popularity. The current adipose tissue harvesting procedures introduce nonphysiological conditions, which may affect the overall performance of the isolated ADSCs. In this study, we elucidate the differences between ADSCs isolated from
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Clinical and basic science applications using adipose-derived stem cells (ADSCs) are gaining popularity. The current adipose tissue harvesting procedures introduce nonphysiological conditions, which may affect the overall performance of the isolated ADSCs. In this study, we elucidate the differences between ADSCs isolated from adipose tissues harvested within the first 5 min of the initial surgical incision (well-vascularized, nonpremedicated condition) versus those isolated from adipose tissues subjected to medications and deprived of blood supply during elective free flap procedures (ischemic condition). ADSCs isolated from well-vascularized and ischemic tissues positively immunostained for several standard stem cell markers. Interestingly, the percent change in the CD36 expression for ADSCs isolated from ischemic versus well-vascularized tissue was significantly lower in males than females (p < 0.05). Upon differentiation and maturation to adipocytes, spheroids formed using ADSCs isolated from ischemic adipose tissue had lower triglyceride content compared to those formed using ADSCs isolated from the well-vascularized tissue (p < 0.05). These results indicate that ADSCs isolated from ischemic tissue either fail to uptake fatty acids or fail to efficiently convert those fatty acids into triglycerides. Therefore, more robust ADSCs suitable to establish in vitro adipose tissue models can be obtained by harvesting well-vascularized and nonpremedicated adipose tissues.
Full article
(This article belongs to the Special Issue Human Stem Cells in Disease Modelling and Treatment)
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Open AccessArticle
Microbial Signatures in COVID-19: Distinguishing Mild and Severe Disease via Gut Microbiota
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Julia S. Galeeva, Dmitry E. Fedorov, Elizaveta V. Starikova, Alexander I. Manolov, Alexander V. Pavlenko, Oksana V. Selezneva, Ksenia M. Klimina, Vladimir A. Veselovsky, Maxim D. Morozov, Oleg O. Yanushevich, Natella I. Krikheli, Oleg V. Levchenko, Dmitry N. Andreev, Filipp S. Sokolov, Aleksey K. Fomenko, Mikhail K. Devkota, Nikolai G. Andreev, Andrey V. Zaborovskiy, Petr A. Bely, Sergei V. Tsaregorodtsev, Vladimir V. Evdokimov, Igor V. Maev, Vadim M. Govorun and Elena N. Ilinaadd
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Biomedicines 2024, 12(5), 996; https://doi.org/10.3390/biomedicines12050996 (registering DOI) - 01 May 2024
Abstract
The COVID-19 pandemic, caused by the SARS-CoV-2 virus, has significantly impacted global healthcare, underscoring the importance of exploring the virus’s effects on infected individuals beyond treatments and vaccines. Notably, recent findings suggest that SARS-CoV-2 can infect the gut, thereby altering the gut microbiota.
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The COVID-19 pandemic, caused by the SARS-CoV-2 virus, has significantly impacted global healthcare, underscoring the importance of exploring the virus’s effects on infected individuals beyond treatments and vaccines. Notably, recent findings suggest that SARS-CoV-2 can infect the gut, thereby altering the gut microbiota. This study aimed to analyze the gut microbiota composition differences between COVID-19 patients experiencing mild and severe symptoms. We conducted 16S rRNA metagenomic sequencing on fecal samples from 49 mild and 43 severe COVID-19 cases upon hospital admission. Our analysis identified a differential abundance of specific bacterial species associated with the severity of the disease. Severely affected patients showed an association with Enterococcus faecium, Akkermansia muciniphila, and others, while milder cases were linked to Faecalibacterium prausnitzii, Alistipes putredinis, Blautia faecis, and additional species. Furthermore, a network analysis using SPIEC-EASI indicated keystone taxa and highlighted structural differences in bacterial connectivity, with a notable disruption in the severe group. Our study highlights the diverse impacts of SARS-CoV-2 on the gut microbiome among both mild and severe COVID-19 patients, showcasing a spectrum of microbial responses to the virus. Importantly, these findings align, to some extent, with observations from other studies on COVID-19 gut microbiomes, despite variations in methodologies. The findings from this study, based on retrospective data, establish a foundation for future prospective research to confirm the role of the gut microbiome as a predictive biomarker for the severity of COVID-19.
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(This article belongs to the Special Issue Gut Microbiota, Diet, and Immunity: Investigating the Connections and Implications for Disease Development)
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Open AccessArticle
Cellular and Structural Changes in Achilles and Patellar Tendinopathies: A Pilot In Vivo Study
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Dimitrios Kouroupis, Carlotta Perucca Orfei, Diego Correa, Giuseppe Talò, Francesca Libonati, Paola De Luca, Vincenzo Raffo, Thomas M. Best and Laura de Girolamo
Biomedicines 2024, 12(5), 995; https://doi.org/10.3390/biomedicines12050995 (registering DOI) - 30 Apr 2024
Abstract
Tendinopathies continue to be a challenge for both patients and the medical teams providing care as no universal clinical practice guidelines have been established. In general, tendinopathies are typically characterized by prolonged, localized, activity-related pain with abnormalities in tissue composition, cellularity, and microstructure
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Tendinopathies continue to be a challenge for both patients and the medical teams providing care as no universal clinical practice guidelines have been established. In general, tendinopathies are typically characterized by prolonged, localized, activity-related pain with abnormalities in tissue composition, cellularity, and microstructure that may be observed on imaging or histology. In the lower limb, tendinopathies affecting the Achilles and the patellar tendons are the most common, showing a high incidence in athletic populations. Consistent diagnosis and management have been challenged by a lack of universal consensus on the pathophysiology and clinical presentation. Current management is primarily based on symptom relief and often consists of medications such as non-steroidal anti-inflammatories, injectable therapies, and exercise regimens that typically emphasize progressive eccentric loading of the affected structures. Implementing the knowledge of tendon stem/progenitor cells (TSPCs) and assessing their potential in enhancing tendon repair could fill an important gap in this regard. In the present pilot in vivo study, we have characterized the structural and cellular alterations that occur soon after tendon insult in models of both Achilles and patellar tendinopathy. Upon injury, CD146+ TSPCs are recruited from the interfascicular tendon matrix to the vicinity of the paratenon, whereas the observed reduction in M1 macrophage polarization is related to a greater abundance of reparative CD146+ TSPCs in situ. The robust TSPCs’ immunomodulatory effects on macrophages were also demonstrated in in vitro settings where TSPCs can effectively polarize M1 macrophages towards an anti-inflammatory therapeutic M2 phenotype. Although preliminary, our findings suggest CD146+ TSPCs as a key phenotype that could be explored in the development of targeted regenerative therapies for tendinopathies.
Full article
(This article belongs to the Special Issue Recent Advances in Arthritis and Tendinopathy)
Open AccessArticle
Biogenic Synthesis of Selenium and Copper Oxide Nanoparticles and Inhibitory Effect against Multi-Drug Resistant Biofilm-Forming Bacterial Pathogens
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Rida Rasheed, Abhijnan Bhat, Baljit Singh and Furong Tian
Biomedicines 2024, 12(5), 994; https://doi.org/10.3390/biomedicines12050994 (registering DOI) - 30 Apr 2024
Abstract
Antimicrobial resistance (AMR), caused by microbial infections, has become a major contributor to morbid rates of mortality worldwide and a serious threat to public health. The exponential increase in resistant pathogen strains including Staphylococcus aureus (S. aureus) and Escherichia coli (
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Antimicrobial resistance (AMR), caused by microbial infections, has become a major contributor to morbid rates of mortality worldwide and a serious threat to public health. The exponential increase in resistant pathogen strains including Staphylococcus aureus (S. aureus) and Escherichia coli (E. coli) poses significant hurdles in the health sector due to their greater resistance to traditional treatments and medicines. Efforts to tackle infectious diseases caused by resistant microbes have prompted the development of novel antibacterial agents. Herein, we present selenium and copper oxide monometallic nanoparticles (Se-MMNPs and CuO-MMNPs), characterized using various techniques and evaluated for their antibacterial potential via disc diffusion, determination of minimum inhibitory concentration (MIC), antibiofilm, and killing kinetic action. Dynamic light scattering (DLS), scanning electron microscopy (SEM/EDX), and X-ray diffraction (XRD) techniques confirmed the size-distribution, spherical-shape, stability, elemental composition, and structural aspects of the synthesized nanoparticles. The MIC values of Se-MMNPs and CuO-MMNPs against S. aureus and E. coli were determined to be 125 μg/mL and 100 μg/mL, respectively. Time–kill kinetics studies revealed that CuO-MMNPs efficiently mitigate the growth of S. aureus and E. coli within 3 and 3.5 h while Se-MMNPs took 4 and 5 h, respectively. Moreover, CuO-MMNPs demonstrated better inhibition compared to Se-MMNPs. Overall, the proposed materials exhibited promising antibacterial activity against S. aureus and E. coli pathogens.
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(This article belongs to the Special Issue Nanobiomaterials with Antimicrobial and Anticancer Applications)
Open AccessArticle
T-Large Granular Lymphocytic Leukemia with Hepatosplenic T-Cell Lymphoma? A Rare Case of Simultaneous Neoplastic T-Cell Clones Highlighted by Flow Cytometry and Review of Literature
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Rossana Libonati, Michela Soda, Teodora Statuto, Luciana Valvano, Fiorella D’Auria, Giovanni D’Arena, Giuseppe Pietrantuono, Oreste Villani, Giovanna Rosaria Mansueto, Simona D’Agostino, Massimo Dante Di Somma, Alessia Telesca and Rocchina Vilella
Biomedicines 2024, 12(5), 993; https://doi.org/10.3390/biomedicines12050993 (registering DOI) - 30 Apr 2024
Abstract
Lymphoproliferative diseases are a heterogeneous set of malignant clonal proliferations of lymphocytes. Despite well-established diagnostic criteria, the diagnosis remains difficult due to their variety in clinical presentation and immunophenotypic profile. Lymphoid T-cell disorders are less common than B-cell entities, and the lack of
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Lymphoproliferative diseases are a heterogeneous set of malignant clonal proliferations of lymphocytes. Despite well-established diagnostic criteria, the diagnosis remains difficult due to their variety in clinical presentation and immunophenotypic profile. Lymphoid T-cell disorders are less common than B-cell entities, and the lack of a clear immunophenotypic characteristic makes their identification hard. Flow cytometry turned out to be a useful tool in diagnosing T-cell disorders and to resolve complicated cases, especially if the number of analyzable neoplastic cells is small. We present a case of a 55-year-old man with simultaneous lymphoproliferative neoplastic T-cell clones, one αβ and the other γδ, identified and characterized by flow cytometry (FC), exploiting the variable expression intensity of specific markers. However, the patient’s rapid decline made it impossible to define a differential diagnosis in order to confirm the identity of the γδ clone, which remains uncertain. This case is added to the few other cases already documented in the literature, characterized by the co-existence of T-large granular lymphocytic leukemia (T-LGLL)-αβ and T-LGLL-γδ/Hepatosplenic T-cell lymphoma (HSTCL). Our case underlines the key role of sensitive diagnostic tools in the assessment of potential relationship between the diagnosis, prognosis, and treatment in the two pathologies.
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(This article belongs to the Special Issue Recent Advances in Lymphoma)
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The Role of Extracellular Vesicles in Metabolic Diseases
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Carlos González-Blanco, Sarai Iglesias-Fortes, Ángela Cristina Lockwood, César Figaredo, Daniela Vitulli and Carlos Guillén
Biomedicines 2024, 12(5), 992; https://doi.org/10.3390/biomedicines12050992 (registering DOI) - 30 Apr 2024
Abstract
Extracellular vesicles represent a group of structures with the capacity to communicate with different cells and organs. This complex network of interactions can regulate multiple physiological processes in the organism. Very importantly, these processes can be altered during the appearance of different diseases
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Extracellular vesicles represent a group of structures with the capacity to communicate with different cells and organs. This complex network of interactions can regulate multiple physiological processes in the organism. Very importantly, these processes can be altered during the appearance of different diseases including cancer, metabolic diseases, etc. In addition, these extracellular vesicles can transport different cargoes, altering the initiation of the disease, driving the progression, or even accelerating the pathogenesis. Then, we have explored the implication of these structures in different alterations such as pancreatic cancer, and in different metabolic alterations such as diabetes and its complications and non-alcoholic fatty liver disease. Finally, we have explored in more detail the communication between the liver and the pancreas. In summary, extracellular vesicles represent a very efficient system for the communication among different tissues and permit an efficient system as biomarkers of the disease, as well as being involved in the extracellular-vesicle-mediated transport of molecules, serving as a potential therapy for different diseases.
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(This article belongs to the Special Issue The Role of Extracellular Vesicles in Hepatic, Pancreatic and Biliary Diseases)
Open AccessArticle
Characterization of a Clinically and Biologically Defined Subgroup of Patients with Autism Spectrum Disorder and Identification of a Tailored Combination Treatment
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Laura Pérez-Cano, Luigi Boccuto, Francesco Sirci, Jose Manuel Hidalgo, Samuel Valentini, Mattia Bosio, Xavier Liogier D’Ardhuy, Cindy Skinner, Lauren Cascio, Sujata Srikanth, Kelly Jones, Carrie Buchanan, Steven A. Skinner, Baltazar Gomez-Mancilla, Jean-Marc Hyvelin, Emre Guney and Lynn Durham
Biomedicines 2024, 12(5), 991; https://doi.org/10.3390/biomedicines12050991 (registering DOI) - 30 Apr 2024
Abstract
Autism spectrum disorder (ASD) is a heterogeneous group of neurodevelopmental disorders (NDDs) with a high unmet medical need. The diagnosis of ASD is currently based on behavior criteria, which overlooks the diversity of genetic, neurophysiological, and clinical manifestations. Failure to acknowledge such heterogeneity
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Autism spectrum disorder (ASD) is a heterogeneous group of neurodevelopmental disorders (NDDs) with a high unmet medical need. The diagnosis of ASD is currently based on behavior criteria, which overlooks the diversity of genetic, neurophysiological, and clinical manifestations. Failure to acknowledge such heterogeneity has hindered the development of efficient drug treatments for ASD and other NDDs. DEPI (Databased Endophenotyping Patient Identification) is a systems biology, multi-omics, and machine learning-driven platform enabling the identification of subgroups of patients with NDDs and the development of patient-tailored treatments. In this study, we provide evidence for the validation of a first clinically and biologically defined subgroup of patients with ASD identified by DEPI, ASD Phenotype 1 (ASD-Phen1). Among 313 screened patients with idiopathic ASD, the prevalence of ASD-Phen1 was observed to be ~24% in 84 patients who qualified to be enrolled in the study. Metabolic and transcriptomic alterations differentiating patients with ASD-Phen1 were consistent with an over-activation of NF-κB and NRF2 transcription factors, as predicted by DEPI. Finally, the suitability of STP1 combination treatment to revert such observed molecular alterations in patients with ASD-Phen1 was determined. Overall, our results support the development of precision medicine-based treatments for patients diagnosed with ASD.
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(This article belongs to the Special Issue Diagnostic Biomarkers and Novel Therapeutics Targets for Fragile X Syndrome, Autism Spectrum Disorders and Genetic Neurodevelopmental Diseases: Advances and Challenges)
Open AccessArticle
Effects of Short-, Medium-, and Long-Term Treatment Using Photobiomodulation Therapy Combined with Static Magnetic Field in Aging Rats
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Kadma Karênina Damasceno Soares Monteiro, Shaiane Silva Tomazoni, Gianna Móes Albuquerque Pontes, Adeilson Matias Teixeira, Fernanda Aparecida de Araújo Agra, Carolina Barros Alvim, Sâmela Lopes Medeiros Brigato, Rodrigo Labat Marcos, Humberto Dellê, Andrey Jorge Serra and Ernesto Cesar Pinto Leal-Junior
Biomedicines 2024, 12(5), 990; https://doi.org/10.3390/biomedicines12050990 (registering DOI) - 30 Apr 2024
Abstract
(1) Background: We investigated the detrimental and protective effects of short-, medium, and long-term treatment with different doses of photobiomodulation therapy combined with static magnetic field (PBMT-sMF) during the aging process. (2) Methods: Rats were treated for 15, 30, and 60 weeks with
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(1) Background: We investigated the detrimental and protective effects of short-, medium, and long-term treatment with different doses of photobiomodulation therapy combined with static magnetic field (PBMT-sMF) during the aging process. (2) Methods: Rats were treated for 15, 30, and 60 weeks with 1, 3, 10, and 30 J of PBMT-sMF or a placebo control. In addition, eight young rats were not subjected to any procedure or treatment and were euthanized at six weeks old. Skin, muscle, bone, kidney, liver, and blood samples were analyzed. (3) Results: No differences between the groups in the morphology of the skin, muscle, and bone was observed. Glutamic pyruvic transaminase levels were increased in the placebo group after 30 and 60 weeks. Glutamic oxaloacetic transaminase levels were also increased in the placebo group after 30 weeks. An increase in creatinine in the PBMT-sMF 3, 10, and 30 J groups compared with that in the young control group was observed. No significant difference in urea levels between the groups was noted. Vascular endothelial growth factor increased in the PBMT-sMF 10 and 30 J groups after 15 weeks of treatment and in the PBMT-sMF 3 J after 60 weeks. Finally, vascular endothelial growth factor decreased in the PBMT-sMF 30 J group after 30 weeks of treatment. (4) Conclusions: PBMT-sMF did not have detrimental effects on the skin, muscle, bone, kidney, or liver after short-, medium-, and long-term treatments in aging rats. In addition, PBMT-sMF may have protective effects on the muscle tissue in aging rats after short- and long-term treatment.
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(This article belongs to the Section Neurobiology and Clinical Neuroscience)
Open AccessArticle
Ruscogenin Attenuates Ulcerative Colitis in Mice by Inhibiting Caspase-1-Dependent Pyroptosis via the TLR4/NF-κB Signaling Pathway
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Jingwei Li, Huihuan Wu, Jialiang Zhou, Rui Jiang, Zewei Zhuo, Qi Yang, Hao Chen and Weihong Sha
Biomedicines 2024, 12(5), 989; https://doi.org/10.3390/biomedicines12050989 (registering DOI) - 30 Apr 2024
Abstract
Inflammatory bowel diseases (IBD) are chronic inflammatory disorders affecting the digestive tract, including ulcerative colitis and Crohn’s disease. Ruscogenin, a prominent steroidal sapogenin present in radix ophiopogon japonicus, has shown a protective effect on attenuating the inflammatory response associated with inflammatory
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Inflammatory bowel diseases (IBD) are chronic inflammatory disorders affecting the digestive tract, including ulcerative colitis and Crohn’s disease. Ruscogenin, a prominent steroidal sapogenin present in radix ophiopogon japonicus, has shown a protective effect on attenuating the inflammatory response associated with inflammatory diseases, but the efficacy of ruscogenin in IBD remains unclear. The aim of this study is to explore the effect of ruscogenin on intestinal barrier dysfunction and inflammatory responses as well as the underlying mechanism in ulcerative colitis. A dextran sulfate sodium salt (DSS)-induced C57BL/6 mouse colitis model was employed for the in vivo studies, while in vitro experiments were performed in THP-1 cells and human intestinal epithelial cells involved in inducing inflammatory responses and pyroptosis using LPS/nigericin. The results indicated that ruscogenin treatment attenuated the symptoms of ulcerative colitis, reduced the release of inflammatory cytokines and the expression of pyroptosis-associated proteins, and restored the integrity of the intestinal epithelial barrier in colon tissue in mice. Moreover, ruscogenin inhibited LPS/nigericin-induced pyroptosis in THP-1 cells. Mechanically, ruscogenin inhibited NLRP3 inflammasome activation and canonical pyroptosis, at least in part, through the suppression of the TLR4/NF-κB signaling pathway. These findings might provide new insights and a solid foundation for further exploration into the therapeutic potential of ruscogenin in the treatment of IBD.
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(This article belongs to the Special Issue Crohn's Disease and Ulcerative Colitis: From Pathophysiology to Novel Therapeutic Approaches (2nd Edition))
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Hepatocyte-Specific PEX16 Abrogation in Mice Leads to Hepatocyte Proliferation, Alteration of Hepatic Lipid Metabolism, and Resistance to High-Fat Diet (HFD)-Induced Hepatic Steatosis and Obesity
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Xue Chen, Long Wang, Krista L. Denning, Anna Mazur, Yujuan Xu, Kesheng Wang, Logan M. Lawrence, Xiaodong Wang and Yongke Lu
Biomedicines 2024, 12(5), 988; https://doi.org/10.3390/biomedicines12050988 (registering DOI) - 30 Apr 2024
Abstract
Obesity results in hepatic fat accumulation, i.e., steatosis. In addition to fat overload, impaired fatty acid β-oxidation also promotes steatosis. Fatty acid β-oxidation takes place in the mitochondria and peroxisomes. Usually, very long-chain and branched-chain fatty acids are the first to be oxidized
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Obesity results in hepatic fat accumulation, i.e., steatosis. In addition to fat overload, impaired fatty acid β-oxidation also promotes steatosis. Fatty acid β-oxidation takes place in the mitochondria and peroxisomes. Usually, very long-chain and branched-chain fatty acids are the first to be oxidized in peroxisomes, and the resultant short chain fatty acids are further oxidized in the mitochondria. Peroxisome biogenesis is regulated by peroxin 16 (PEX16). In liver-specific PEX16 knockout (Pex16Alb-Cre) mice, hepatocyte peroxisomes were absent, but hepatocytes proliferated, and liver mass was enlarged. These results suggest that normal liver peroxisomes restrain hepatocyte proliferation and liver sizes. After high-fat diet (HFD) feeding, body weights were increased in PEX16 floxed (Pex16fl/fl) mice and adipose-specific PEX16 knockout (Pex16AdipoQ-Cre) mice, but not in the Pex16Alb-Cre mice, suggesting that the development of obesity is regulated by liver PEX16 but not by adipose PEX16. HFD increased liver mass in the Pex16fl/fl mice but somehow reduced the already enlarged liver mass in the Pex16Alb-Cre mice. The basal levels of serum triglyceride, free fatty acids, and cholesterol were decreased, whereas serum bile acids were increased in the Pex16Alb-Cre mice, and HFD-induced steatosis was not observed in the Pex16Alb-Cre mice. These results suggest that normal liver peroxisomes contribute to the development of liver steatosis and obesity.
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(This article belongs to the Special Issue Interaction between Liver and Adipose Tissues)
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Drug-Induced Myopathies: A Comprehensive Review and Update
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Sebastian Miernik, Agata Matusiewicz and Marzena Olesińska
Biomedicines 2024, 12(5), 987; https://doi.org/10.3390/biomedicines12050987 (registering DOI) - 30 Apr 2024
Abstract
Drug-induced myopathies are a common cause of muscle pain, and the range of drugs that can cause muscle side effects is constantly expanding. In this article, the authors comprehensively discuss the diagnostic and therapeutic process in patients with myalgia, and present the spectrum
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Drug-induced myopathies are a common cause of muscle pain, and the range of drugs that can cause muscle side effects is constantly expanding. In this article, the authors comprehensively discuss the diagnostic and therapeutic process in patients with myalgia, and present the spectrum of drug-induced myopathies. The review provides a detailed analysis of the literature on the incidence of myopathy during treatment with hypolipemic drugs, beta-blockers, amiodarone, colchicine, glucocorticosteroids, antimalarials, cyclosporine, zidovudine, and checkpoint inhibitors, a group of drugs increasingly used in the treatment of malignancies. The article considers the clinical course of the different types of myopathies, their pathogenesis, histopathological features, and treatment methods of these disorders. The aim of this paper is to gather from the latest available literature up-to-date information on the course, pathophysiology, and therapeutic options of drug-induced myopathies, to systematize the knowledge of drug-induced myopathies and to draw the attention of internists to the fact that these clinical issues are an important therapeutic problem.
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(This article belongs to the Special Issue State-of-the-Art Drug Discovery and Development in Poland)
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The Impact of Medical Physical Training and a Structured Personalized Exercise Training Program on Hemodynamic Parameters and Arterial Stiffness in Pregnant Women
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Izabella Petre, Stela Iurciuc, Florina Buleu, Ion Petre, Radu Dumitru Moleriu, Daian Popa, Vladiana Turi, Anca Bordianu, Rabia Tasdemir, Laura Maria Craciun, Luciana Marc, Flavia Mirela Barna and Mircea Iurciuc
Biomedicines 2024, 12(5), 986; https://doi.org/10.3390/biomedicines12050986 (registering DOI) - 30 Apr 2024
Abstract
Introduction: In developed countries, heart disease is the primary cause of maternal mortality during pregnancy. Arterial stiffness, an independent risk factor for atherosclerosis and a predictor of cardiovascular complications, can be assessed using the augmentation index (AIx) and pulse wave velocity (PWV). In
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Introduction: In developed countries, heart disease is the primary cause of maternal mortality during pregnancy. Arterial stiffness, an independent risk factor for atherosclerosis and a predictor of cardiovascular complications, can be assessed using the augmentation index (AIx) and pulse wave velocity (PWV). In this prospective study, we aimed to evaluate diverse hemodynamic parameters and arterial stiffness in pregnant women before and after participating in a structured, personalized exercise training program. Materials and methods: Forty healthy pregnant women, non-smokers, who agreed to participate daily for 12 weeks in a physical exercise training program under the supervision of a team made up of an obstetrician, a cardiologist, and a physiotherapist were included. Anthropometric characteristics, arterial function, and physical activity data were collected from the participants at two different time points: at the beginning of the exercise training program (T0) and at the end, after 12 weeks (T1). Results: Upon conducting a statistical analysis, it was discovered that there were noteworthy disparities (p = 0.05) in body mass index, brachial AIx, systolic blood pressure, and pulse pressure values between the two time points. The regression analysis for the AIx brachial values and the PWVao values from Trim II (T0) and Trim III (T1) showed major differences between these two time points; the association between the AIx brachial values in the second and third trimesters of pregnancy revealed a strong direct significant correlation (p < 0.001), and the correlation between the PWVao values in the second (T0) and third trimester (T1) of pregnancy was weak and insignificant (p = 0.12). Conclusions: The findings of our study indicate that a personalized exercise training program positively impacts the physical and psychological well-being of pregnant women, leading to a reduction in PWV.
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(This article belongs to the Special Issue Connections between Diabetes Mellitus, Other Metabolic and Endocrine Dysfunctions and Cardiovascular Pathologies)
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Endurance Training Provokes Arrhythmogenic Right Ventricular Cardiomyopathy Phenotype in Heterozygous Desmoglein-2 Mutants: Alleviation by Preload Reduction
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Larissa Fabritz, Lisa Fortmueller, Katja Gehmlich, Sebastian Kant, Marcel Kemper, Dana Kucerova, Fahima Syeda, Cornelius Faber, Rudolf E. Leube, Paulus Kirchhof and Claudia A. Krusche
Biomedicines 2024, 12(5), 985; https://doi.org/10.3390/biomedicines12050985 (registering DOI) - 30 Apr 2024
Abstract
Desmoglein-2 mutations are detected in 5–10% of patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). Endurance training accelerates the development of the ARVC phenotype, leading to earlier arrhythmic events. Homozygous Dsg2 mutant mice develop a severe ARVC-like phenotype. The phenotype of heterozygous mutant (
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Desmoglein-2 mutations are detected in 5–10% of patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). Endurance training accelerates the development of the ARVC phenotype, leading to earlier arrhythmic events. Homozygous Dsg2 mutant mice develop a severe ARVC-like phenotype. The phenotype of heterozygous mutant (Dsg2mt/wt) or haploinsufficient (Dsg20/wt) mice is still not well understood. To assess the effects of age and endurance swim training, we studied cardiac morphology and function in sedentary one-year-old Dsg2mt/wt and Dsg20/wt mice and in young Dsg2mt/wt mice exposed to endurance swim training. Cardiac structure was only occasionally affected in aged Dsg20/wt and Dsg2mt/wt mice manifesting as small fibrotic foci and displacement of Connexin 43. Endurance swim training increased the right ventricular (RV) diameter and decreased RV function in Dsg2mt/wt mice but not in wild types. Dsg2mt/wt hearts showed increased ventricular activation times and pacing-induced ventricular arrhythmia without obvious fibrosis or inflammation. Preload-reducing therapy during training prevented RV enlargement and alleviated the electrophysiological phenotype. Taken together, endurance swim training induced features of ARVC in young adult Dsg2mt/wt mice. Prolonged ventricular activation times in the hearts of trained Dsg2mt/wt mice are therefore a potential mechanism for increased arrhythmia risk. Preload-reducing therapy prevented training-induced ARVC phenotype pointing to beneficial treatment options in human patients.
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(This article belongs to the Special Issue Advanced Research in Arrhythmogenic Cardiomyopathy)
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Open AccessReview
Recent Data about the Use of Corticosteroids in Sepsis—Review of Recent Literature
by
Alexandra Lazar
Biomedicines 2024, 12(5), 984; https://doi.org/10.3390/biomedicines12050984 (registering DOI) - 30 Apr 2024
Abstract
Sepsis, characterized by life-threatening organ dysfunction due to a maladaptive host response to infection, and its more severe form, septic shock, pose significant global health challenges. The incidence of these conditions is increasing, highlighting the need for effective treatment strategies. This review explores
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Sepsis, characterized by life-threatening organ dysfunction due to a maladaptive host response to infection, and its more severe form, septic shock, pose significant global health challenges. The incidence of these conditions is increasing, highlighting the need for effective treatment strategies. This review explores the complex pathophysiology of sepsis, emphasizing the role of the endothelium and the therapeutic potential of corticosteroids. The endothelial glycocalyx, critical in maintaining vascular integrity, is compromised in sepsis, leading to increased vascular permeability and organ dysfunction. Corticosteroids have been used for over fifty years to treat severe infections, despite ongoing debate about their efficacy. Their immunosuppressive effects and the risk of exacerbating infections are significant concerns. The rationale for corticosteroid use in sepsis is based on their ability to modulate the immune response, promote cardiovascular stability, and potentially facilitate organ restoration. However, the evidence is mixed, with some studies suggesting benefits in terms of microcirculation and shock reversal, while others report no significant impact on mortality or organ dysfunction. The Surviving Sepsis Campaign provides cautious recommendations for their use. Emerging research highlights the importance of genomic and transcriptomic analyses in identifying patient subgroups that may benefit from corticosteroid therapy, suggesting a move toward personalized medicine in sepsis management. Despite potential benefits, the use of corticosteroids in sepsis requires careful consideration of individual patient risk profiles, and further research is needed to optimize their use and integrate genomic insights into clinical practice. This review underscores the complexity of sepsis treatment and the ongoing need for evidence-based approaches to improve patient outcomes.
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(This article belongs to the Special Issue Molecular Biomarkers and More Efficient Therapies for Sepsis)
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Chemerin Levels in Individuals with Type 2 Diabetes and a Normal Weight versus Individuals with Type 2 Diabetes and Obesity: An Observational, Cross-Sectional Study
by
Aishee B. Mukherji, Victoria Idowu, Lei Zhao, Lawrence L. K. Leung, Sa Shen, Latha Palaniappan and John Morser
Biomedicines 2024, 12(5), 983; https://doi.org/10.3390/biomedicines12050983 (registering DOI) - 30 Apr 2024
Abstract
Chemerin acts as both a chemotactic agent and an adipokine that undergoes proteolytic cleavage, converting inactive precursors into their active forms before being subsequently inactivated. Elevated chemerin levels are linked to obesity and type 2 diabetes mellitus (T2D). This study aimed to elucidate
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Chemerin acts as both a chemotactic agent and an adipokine that undergoes proteolytic cleavage, converting inactive precursors into their active forms before being subsequently inactivated. Elevated chemerin levels are linked to obesity and type 2 diabetes mellitus (T2D). This study aimed to elucidate the effects of T2D and obesity on chemerin levels by comparing plasma samples from individuals with a normal weight and T2D (BMI < 25; NWD group n = 22) with those from individuals who are overweight or obese and have T2D (BMI ≥ 25; OWD group n = 39). The total chemerin levels were similar in the NWD and OWD groups, suggesting that T2D may equalize the chemerin levels irrespective of obesity status. The cleavage of chemerin has been previously linked to myocardial infarction and stroke in NWD, with potential implications for inflammation and mortality. OWD plasma exhibited lower levels of cleaved chemerin than the NWD group, suggesting less inflammation in the OWD group. Here, we showed that the interaction between obesity and T2D leads to an equalization in the total chemerin levels. The cleaved chemerin levels and the associated inflammatory state, however, differ significantly, underscoring the complex relationship between chemerin, T2D, and obesity.
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(This article belongs to the Special Issue Recent Advances in Adipokines—2nd Edition)
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Beyond the Biomarker: Unveiling the Multifaceted Role of Osteopontin in Both Physiological and Pathological Processes
by
Davide Raineri, Annalisa Chiocchetti and Giuseppe Cappellano
Biomedicines 2024, 12(5), 982; https://doi.org/10.3390/biomedicines12050982 (registering DOI) - 30 Apr 2024
Abstract
Osteopontin (OPN), a multifunctional protein, has emerged as a fascinating subject of study due to its diverse roles in various physiological and pathological processes [...]
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(This article belongs to the Special Issue 30 Years of OPN Milestones and Future Avenues)
Open AccessReview
Pathophysiological Link and Treatment Implication of Heart Failure and Preserved Ejection Fraction in Patients with Chronic Kidney Disease
by
Giacomo Bonacchi, Valentina Alice Rossi, Manuel Garofalo, Rocco Mollace, Giuseppe Uccello, Paolo Pieragnoli, Luca Checchi, Laura Perrotta, Luca Voltolini, Giuseppe Ricciardi and Matteo Beltrami
Biomedicines 2024, 12(5), 981; https://doi.org/10.3390/biomedicines12050981 (registering DOI) - 30 Apr 2024
Abstract
Heart failure with preserved ejection fraction (HFpEF) results from a complex interplay of age, genetic, cardiac remodeling, and concomitant comorbidities including hypertension, obesity, diabetes, and chronic kidney disease (CKD). Renal failure is an important comorbidity of HFpEF, as well as a major pathophysiological
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Heart failure with preserved ejection fraction (HFpEF) results from a complex interplay of age, genetic, cardiac remodeling, and concomitant comorbidities including hypertension, obesity, diabetes, and chronic kidney disease (CKD). Renal failure is an important comorbidity of HFpEF, as well as a major pathophysiological mechanism for those patients at risk of developing HFpEF. Heart failure (HF) and CKD are intertwined conditions sharing common disease pathways; the so-called “kidney tamponade”, explained by an increase in intracapsular pressure caused by fluid retention, is only the latest model to explain renal injury in HF. Recognizing the different phenotypes of HFpEF remains a real challenge; the pathophysiological mechanisms of renal dysfunction may differ across the HF spectrum, as well as the prognostic role. A better understanding of the role of cardiorenal interactions in patients with HF in terms of symptom status, disease progression, and prognosis remains essential in HF management. Historically, patients with HF and CKD have been scarcely represented in clinical trial populations. Current concerns affect the practical approach to HF treatment, and, in this context, physicians are frequently hesitant to prescribe and titrate both new and old treatments. Therefore, the extensive application of HF drugs in diverse HF subtypes with numerous comorbidities and different renal dysfunction etiologies remains a controversial matter of discussion. Numerous recently introduced drugs, such as sodium–glucose-linked transporter 2 inhibitors (SGLT2i), constitute a new therapeutic option for patients with HF and CKD. Because of their protective vascular and hormonal actions, the use of these agents may be safely extended to patients with renal dysfunction in the long term. The present review delves into the phenotype of patients with HFpEF and CKD from a pathophysiological perspective, proposing a treatment approach that suggests a practical stepwise algorithm for the proper application of life-saving therapies in clinical practice.
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(This article belongs to the Special Issue Pathophysiology of Chronic Kidney Disease and Its Complications 2nd Edition)
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The Interleukin-15 and Interleukin-8 Axis as a Novel Mechanism for Recurrent Chronic Rhinosinusitis with Nasal Polyps
by
Kai-Min Fang, Yen-Ling Chiu, Ruo-Wei Hong, Ping-Chia Cheng, Po-Wen Cheng and Li-Jen Liao
Biomedicines 2024, 12(5), 980; https://doi.org/10.3390/biomedicines12050980 (registering DOI) - 29 Apr 2024
Abstract
The prevention of postoperative recurrence after endoscopic sinus surgery (ESS) relies on targeting specific pathological mechanisms according to individuals’ immunological profiles. However, essential biomarkers and biological characteristics of difficult-to-treat chronic rhinosinusitis (CRS) patients are not well-defined. The aim of this study was to
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The prevention of postoperative recurrence after endoscopic sinus surgery (ESS) relies on targeting specific pathological mechanisms according to individuals’ immunological profiles. However, essential biomarkers and biological characteristics of difficult-to-treat chronic rhinosinusitis (CRS) patients are not well-defined. The aim of this study was to explore the immunologic profiles of subgroups of CRS patients and determine the specific cytokines responsible for recalcitrant or recurrent CRS with nasal polyposis (rCRSwNP). We used 30 cytokine antibody arrays to determine the key cytokines related to recurrent polypogenesis. Enzyme-linked immunosorbent assay (ELISA) experiments were conducted to assess the levels of these key cytokines in 78 patients. Polymorphonuclear leukocytes (PMNs) isolated from nasal polyps were challenged with specific cytokines to examine the levels of enhanced interleukin (IL)-8 production. Finally, we used immunohistochemistry (IHC) staining to check for the presence and distribution of the biomarkers within nasal polyps. A cytokine antibody array revealed that IL-8, IL-13, IL-15, and IL-20 were significantly higher in the recalcitrant CRSwNP group. Subsequent ELISA screening showed a stepwise increase in tissue IL-8 levels in the CHR, CRSsNP, and CRSwNP groups. PMNs isolated from nine CRSwNP cases all demonstrated enhanced IL-8 production after IL-15 treatment. IHC staining was labeled concurrent IL-8 and IL-15 expression in areas of prominent neutrophil infiltration. Our results suggest that IL-15 within the sinonasal mucosa plays a crucial role in promoting IL-8 secretion by infiltrating PMNs in recalcitrant nasal polyps. In addition, we propose a novel therapeutic strategy targeting the anti-IL-15/IL-8 axis to treat CRS with nasal polyposis.
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(This article belongs to the Section Immunology and Immunotherapy)
Open AccessArticle
High PGC-1α Expression as a Poor Prognostic Indicator in Intracranial Glioma
by
Yu-Wen Cheng, Jia-Hau Lee, Chih-Hui Chang, Tzu-Ting Tseng, Chee-Yin Chai, Ann-Shung Lieu and Aij-Lie Kwan
Biomedicines 2024, 12(5), 979; https://doi.org/10.3390/biomedicines12050979 (registering DOI) - 29 Apr 2024
Abstract
Gliomas are the most common primary brain tumors in adults. Despite multidisciplinary treatment approaches, the survival rates for patients with malignant glioma have only improved marginally, and few prognostic biomarkers have been identified. Peroxisome proliferator-activated receptor γ (PPARγ) coactivator-1α (PGC-1α) is a crucial
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Gliomas are the most common primary brain tumors in adults. Despite multidisciplinary treatment approaches, the survival rates for patients with malignant glioma have only improved marginally, and few prognostic biomarkers have been identified. Peroxisome proliferator-activated receptor γ (PPARγ) coactivator-1α (PGC-1α) is a crucial regulator of cancer metabolism, playing a vital role in cancer cell adaptation to fluctuating energy demands. In this study, the clinicopathological roles of PGC-1α in gliomas were evaluated. Employing immunohistochemistry, cell culture, siRNA transfection, cell viability assays, western blot analyses, and in vitro and in vivo invasion and migration assays, we explored the functions of PGC-1α in glioma progression. High PGC-1α expression was significantly associated with an advanced pathological stage in patients with glioma and with poorer overall survival. The downregulation of PGC-1α inhibited glioma cell proliferation, invasion, and migration and altered the expression of oncogenic markers. These results conclusively demonstrated that PGC-1α plays a critical role in maintaining the malignant phenotype of glioma cells and indicated that targeting PGC-1α could be an effective strategy to curb glioma progression and improve patient survival outcomes.
Full article
(This article belongs to the Special Issue Gliomas: Signaling Pathways, Molecular Mechanisms and Novel Therapies)
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