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Recent Advances in Metabolism and Oxidative Stress in Human Diseases
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Recent Advances in Metabolism and Oxidative Stress in Human Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: closed (28 February 2023) | Viewed by 19853

Special Issue Editor

Dr. Isabella Panfoli

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Guest Editor
Dipartimento di Farmacia (DIFAR), Università degli Studi di Genova, Scuola di Scienze Mediche e Farmaceutiche, V.le Benedetto XV, 3, 16132 Genoa, Italy
Interests: bioenergetics; neurosciences; metabolism; photoreceptors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolism, the series of reactions that occur in living cells, involves many interconnected cellular pathways that ultimately provide cells with chemical energy in the form of ATP. Most of the cell ATP is produced by mitochondrial oxidative phosphorylation (OxPhos). In turn, the OxPhos efficacy seems to depend on the mitochondrial morphology and number, which likely reflect the metabolic needs of the cell. Mitochondria are dynamic organelles that divide and fuse to form an extensive network. Moreover, recent evidence points to the existence of a connection of the mitochondrial reticulum to the endoplasmic reticulum. Moreover, in the recent years an ectopic OxPhos activity has been described in membranes other than mitochondrial membranes, such as the rod outer segments, the myelin sheath, and the plasma membranes of hepatocytes, cancer and endothelial cells, as well as exosomes, microvesicles and platelets. Mitochondria also play a role in Ca2+ buffering and are the main intracellular sources of reactive oxygen species (ROS), a by-product of oxidative phosphorylation under physiological conditions. Oxidative stress, defined as an imbalance between ROS generation and the endogenous and exogenous antioxidant systems, is emerging as the ultimate cause of several diverse diseases. Oxidative stress is involved in the ageing process and multiple age-related diseases, such as atherosclerosis, cardiovascular diseases (CVDs), and neurodegenerative diseases. Platelets contribute to inflammation and immune responses, and play an important role in cardiovascular disease thrombosis and atherosclerosis. A link exists between Alzheimer’s disease and dysfunctional glucose metabolism. Metabolic reprogramming leads to cellular senescence. Metabolism is profoundly altered in osteoarthritis (OA). The metabolic reprogramming of most core metabolic pathways, including glucose, glutamine, amino acids, and lipids, is a hallmark of cancer cells in the various stages of the disease. The metabolic switch of cancer cells from aerobic glycolysis (Warburg effect) to OxPhos is characteristic of the acquisition of metastasizing features. Endothelial cell metabolism is important in both health and disease, being a determinant of angiogenesis—a process also involved in cancer growth. Metabolic pathways are recognized as important regulators of immune activation, also influencing the development of autoimmune diseases. ROS generation promotes the activation of the mechanistic target of rapamycin (mTOR), in turn a metabolic sensor. Understanding the mechanisms of metabolic reprogramming, thereby including mitochondrial function and biology, has the potential to lead to the development of effective treatments for a number of diseases.

Dr. Isabella Panfoli
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • ageing
  • atherosclerosis
  • atp
  • autoimmune diseases
  • cardiovascular disease
  • cancer cells
  • endoplasmic reticulum
  • endothelial cells
  • inflammation
  • mitochondria
  • mitochondrial dynamics
  • metabolic reprogramming
  • metabolism
  • mitophagy
  • neurodegeneration
  • reactive oxygen species
  • oxidative phosphorylation
  • platelets

Related Special Issues

Published Papers (10 papers)

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Editorial

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4 pages, 200 KiB  
Editorial
The Liaison between Metabolism and Oxidative Stress in Human Diseases
by Silvia Ravera and Isabella Panfoli
Cells 2023, 12(24), 2823; https://doi.org/10.3390/cells12242823 - 12 Dec 2023
Viewed by 630
Abstract
Mitochondria have been the prerequisite to eukaryote complexity since their likely endosymbiotic origin, allowing a remarkable expansion in the number of genes expressed [...] Full article
(This article belongs to the Special Issue Recent Advances in Metabolism and Oxidative Stress in Human Diseases)

Research

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15 pages, 2885 KiB  
Article
Crosstalk between the Rod Outer Segments and Retinal Pigmented Epithelium in the Generation of Oxidative Stress in an In Vitro Model
by Silvia Ravera, Nadia Bertola, Alessandra Puddu, Silvia Bruno, Davide Maggi and Isabella Panfoli
Cells 2023, 12(17), 2173; https://doi.org/10.3390/cells12172173 - 30 Aug 2023
Cited by 1 | Viewed by 982
Abstract
Dysfunction of the retinal pigment epithelium (RPE) is associated with several diseases characterized by retinal degeneration, such as diabetic retinopathy (DR). However, it has recently been proposed that outer retinal neurons also participate in the damage triggering. Therefore, we have evaluated the possible [...] Read more.
Dysfunction of the retinal pigment epithelium (RPE) is associated with several diseases characterized by retinal degeneration, such as diabetic retinopathy (DR). However, it has recently been proposed that outer retinal neurons also participate in the damage triggering. Therefore, we have evaluated the possible crosstalk between RPE and photoreceptors in priming and maintaining oxidative damage of the RPE. For this purpose, we used ARPE-19 cells as a model of human RPE, grown in normal (NG, 5.6 mM) or high glucose (HG, 25 mM) and unoxidized (UOx) or oxidized (Ox) mammalian retinal rod outer segments (OSs). ARPE-19 cells were efficient at phagocytizing rod OSs in both NG and HG settings. However, in HG, ARPE-19 cells treated with Ox-rod OSs accumulated MDA and lipofuscins and displayed altered LC3, GRP78, and caspase 8 expression compared to untreated and UOx-rod-OS-treated cells. Data suggest that early oxidative damage may originate from the photoreceptors and subsequently extend to the RPE, providing a new perspective to the idea that retinal degeneration depends solely on a redox alteration of the RPE. Full article
(This article belongs to the Special Issue Recent Advances in Metabolism and Oxidative Stress in Human Diseases)
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14 pages, 1544 KiB  
Article
Oxidative Stress and Inflammation Biomarkers in Postoperative Pain Modulation in Surgically Treated Patients with Laryngeal Cancer—Pilot Study
by Katarina Savic Vujovic, Andjela Zivkovic, Ivan Dozic, Andja Cirkovic, Branislava Medic, Dragana Srebro, Sonja Vuckovic, Jovica Milovanovic and Ana Jotic
Cells 2023, 12(10), 1391; https://doi.org/10.3390/cells12101391 - 14 May 2023
Viewed by 1791
Abstract
(1) Background: Surgical treatment of laryngeal carcinoma includes different types of laryngectomies with neck dissection. Surgical tissue damage triggers an inflammatory response, leading to the release of pro-inflammatory molecules. This increases reactive oxygen species production and decreases antioxidant defense mechanisms, leading to postoperative [...] Read more.
(1) Background: Surgical treatment of laryngeal carcinoma includes different types of laryngectomies with neck dissection. Surgical tissue damage triggers an inflammatory response, leading to the release of pro-inflammatory molecules. This increases reactive oxygen species production and decreases antioxidant defense mechanisms, leading to postoperative oxidative stress. The aim of this study was to assess the correlation between oxidative stress (malondialdehyde, MDA; glutathione peroxidase, GPX; superoxide dismutase, SOD) and inflammation (interleukin 1, IL-1; interleukin-6, IL-6; C–reactive protein, CRP) parameters and postoperative pain management in patients surgically treated with laryngeal cancer. (2) Methods: This prospective study included 28 patients with surgically treated laryngeal cancer. Blood samples were taken for the analysis of oxidative stress and inflammation parameters before the operative treatment and after the operative treatment (1st postoperative day and 7th postoperative day). The concentrations of MDA, SOD, GPX, IL-1, IL-6, and CRP in the serum were determined by coated enzyme-linked immunosorbent assay (ELISA). The visual analog scale (VAS) was used for pain assessment. (3) Results and conclusion: There was a correlation between oxidative stress and inflammation biomarkers and postoperative pain modulation in surgically treated patients with laryngeal cancer. Age, more extensive surgery, CRP values, and use of tramadol were predictors for oxidative stress parameters. Full article
(This article belongs to the Special Issue Recent Advances in Metabolism and Oxidative Stress in Human Diseases)
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15 pages, 2948 KiB  
Article
The Flavone Cirsiliol from Salvia x jamensis Binds the F1 Moiety of ATP Synthase, Modulating Free Radical Production
by Lavinia Carlini, Gabriele Tancreda, Valeria Iobbi, Federico Caicci, Silvia Bruno, Alfonso Esposito, Daniela Calzia, Stefano Benini, Angela Bisio, Lucia Manni, Anna Schito, Carlo Enrico Traverso, Silvia Ravera and Isabella Panfoli
Cells 2022, 11(19), 3169; https://doi.org/10.3390/cells11193169 - 9 Oct 2022
Cited by 9 | Viewed by 1782
Abstract
Several studies have shown that mammalian retinal rod outer segments (OS) are peculiar structures devoid of mitochondria, characterized by ectopic expression of the molecular machinery for oxidative phosphorylation. Such ectopic aerobic metabolism would provide the chemical energy for the phototransduction taking place in [...] Read more.
Several studies have shown that mammalian retinal rod outer segments (OS) are peculiar structures devoid of mitochondria, characterized by ectopic expression of the molecular machinery for oxidative phosphorylation. Such ectopic aerobic metabolism would provide the chemical energy for the phototransduction taking place in the OS. Natural polyphenols include a large variety of molecules having pleiotropic effects, ranging from anti-inflammatory to antioxidant and others. Our goal in the present study was to investigate the potential of the flavonoid cirsiliol, a trihydroxy-6,7-dimethoxyflavone extracted from Salvia x jamensis, in modulating reactive oxygen species production by the ectopic oxidative phosphorylation taking place in the OS. Our molecular docking analysis identified cirsiliol binding sites inside the F1 moiety of the nanomotor F1Fo-ATP synthase. The experimental approach was based on luminometry, spectrophotometry and cytofluorimetry to evaluate ATP synthesis, respiratory chain complex activity and H2O2 production, respectively. The results showed significant dose-dependent inhibition of ATP production by cirsiliol. Moreover, cirsiliol was effective in reducing the free radical production by the OS exposed to ambient light. We report a considerable protective effect of cirsiliol on the structural stability of rod OS, suggesting it may be considered a promising compound against oxidative stress. Full article
(This article belongs to the Special Issue Recent Advances in Metabolism and Oxidative Stress in Human Diseases)
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16 pages, 1971 KiB  
Article
Mutated FANCA Gene Role in the Modulation of Energy Metabolism and Mitochondrial Dynamics in Head and Neck Squamous Cell Carcinoma
by Nadia Bertola, Paolo Degan, Enrico Cappelli and Silvia Ravera
Cells 2022, 11(15), 2353; https://doi.org/10.3390/cells11152353 - 30 Jul 2022
Cited by 3 | Viewed by 1882
Abstract
Fanconi Anaemia (FA) is a rare recessive genetic disorder characterized by a defective DNA repair mechanism. Although aplastic anaemia is the principal clinical sign in FA, patients develop a head and neck squamous cell carcinoma (HNSCC) with a frequency 500–700 folds higher than [...] Read more.
Fanconi Anaemia (FA) is a rare recessive genetic disorder characterized by a defective DNA repair mechanism. Although aplastic anaemia is the principal clinical sign in FA, patients develop a head and neck squamous cell carcinoma (HNSCC) with a frequency 500–700 folds higher than the general population, which appears more aggressive, with survival of under two years. Since FA gene mutations are also associated with a defect in the aerobic metabolism and an increased oxidative stress accumulation, this work aims to evaluate the effect of FANCA mutation on the energy metabolism and the relative mitochondrial quality control pathways in an HNSCC cellular model. Energy metabolism and cellular antioxidant capacities were evaluated by oximetric, luminometric, and spectrophotometric assays. The dynamics of the mitochondrial network, the quality of mitophagy and autophagy, and DNA double-strand damage were analysed by Western blot analysis. Data show that the HNSCC cellular model carrying the FANCA gene mutation displays an altered electron transport between respiratory Complexes I and III that does not depend on the OxPhos protein expression. Moreover, FANCA HNSCC cells show an imbalance between fusion and fission processes and alterations in autophagy and mitophagy pathways. Together, all these alterations associated with the FANCA gene mutation cause cellular energy depletion and a metabolic switch to glycolysis, exacerbating the Warburg effect in HNSCC cells and increasing the growth rate. In addition, the altered DNA repair due to the FANCA mutation causes a higher accumulation of DNA damage in the HNSCC cellular model. In conclusion, changes in energy metabolism and mitochondrial dynamics could explain the strict correlation between HNSCC and FA genes, helping to identify new therapeutic targets. Full article
(This article belongs to the Special Issue Recent Advances in Metabolism and Oxidative Stress in Human Diseases)
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23 pages, 4038 KiB  
Article
Overexpression of Renin-B Induces Warburg-like Effects That Are Associated with Increased AKT/mTOR Signaling
by Janine Golchert, Doreen Staar, Jonathan Bennewitz, Miriam Hartmann, Nadin Hoffmann, Sabine Ameling, Uwe Völker, Jörg Peters and Heike Wanka
Cells 2022, 11(9), 1459; https://doi.org/10.3390/cells11091459 - 26 Apr 2022
Cited by 1 | Viewed by 1977
Abstract
The classical secretory renin-a is known to be involved in angiotensin generation, thereby regulating not only blood pressure, but also promoting oxidative stress as well as apoptotic and necrotic cell death. In contrast, another cytosolic renin isoform named renin-b has been described, exerting [...] Read more.
The classical secretory renin-a is known to be involved in angiotensin generation, thereby regulating not only blood pressure, but also promoting oxidative stress as well as apoptotic and necrotic cell death. In contrast, another cytosolic renin isoform named renin-b has been described, exerting protective effects under ischemia-related conditions in H9c2 cardiomyoblasts. Using microarray-based transcriptome analyses, we aimed to identify the signaling pathways involved in mediating cardioprotection in H9c2 cells overexpressing renin-b. By transcriptome profiling, we identified increased gene expression of several genes encoding glycolytic enzymes and glucose transporters, while the transcript levels of TCA-cycle enzymes were decreased. Complementing data from metabolic analyses revealed enhanced glucose consumption and lactate accumulation due to renin-b overexpression. Renin-b overexpression further stimulated AKT/mTOR signaling, where numerous genes involved in this pathway showed altered transcript levels. For AKT, we also detected enhanced phosphorylation levels by means of Western blotting, suggesting an activation of this kinase. Moreover, analysis of the ROS levels identified an increase in ROS accumulation in renin-b-overexpressing cells. Altogether, our data demonstrate that renin-b overexpression induces the metabolic remodeling of H9c2 cells similar to that seen under oxygen deprivation. This metabolic phenotype exerting so-called aerobic glycolysis is also known as the Warburg effect. Full article
(This article belongs to the Special Issue Recent Advances in Metabolism and Oxidative Stress in Human Diseases)
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15 pages, 1899 KiB  
Article
Mitochondria Bioenergetic Functions and Cell Metabolism Are Modulated by the Bergamot Polyphenolic Fraction
by Cristina Algieri, Chiara Bernardini, Francesca Oppedisano, Debora La Mantia, Fabiana Trombetti, Ernesto Palma, Monica Forni, Vincenzo Mollace, Giovanni Romeo and Salvatore Nesci
Cells 2022, 11(9), 1401; https://doi.org/10.3390/cells11091401 - 20 Apr 2022
Cited by 10 | Viewed by 2293
Abstract
The bergamot polyphenolic fraction (BPF) was evaluated in the F1FO-ATPase activity of swine heart mitochondria. In the presence of a concentration higher than 50 µg/mL BPF, the ATPase activity of F1FO-ATPase, dependent on the natural [...] Read more.
The bergamot polyphenolic fraction (BPF) was evaluated in the F1FO-ATPase activity of swine heart mitochondria. In the presence of a concentration higher than 50 µg/mL BPF, the ATPase activity of F1FO-ATPase, dependent on the natural cofactor Mg2+, increased by 15%, whereas the enzyme activity in the presence of Ca2+ was inhibited by 10%. By considering this opposite BPF effect, the F1FO-ATPase activity involved in providing ATP synthesis in oxidative phosphorylation and triggering mitochondrial permeability transition pore (mPTP) formation has been evaluated. The BPF improved the catalytic coupling of oxidative phosphorylation in the presence of a substrate at the first phosphorylation site, boosting the respiratory control ratios (state 3/state 4) by 25% and 85% with 50 µg/mL and 100 µg/mL BPF, respectively. Conversely, the substrate at the second phosphorylation site led to the improvement of the state 3/state 4 ratios by 15% only with 100 µg/mL BPF. Moreover, the BPF carried out its beneficial effect on the mPTP phenomenon by desensitizing the pore opening. The acute effect of the BPF on the metabolism of porcine aortica endothelial cells (pAECs) showed an ATP rate index greater than one, which points out a prevailing mitochondrial oxidative metabolism with respect to the glycolytic pathway, and this ratio rose by about three times with 100 µg/mL BPF. Consistently, the mitochondrial ATP turnover, in addition to the basal and maximal respiration, were higher in the presence of the BPF than in the controls, and the MTT test revealed an increase in cell viability with a BPF concentration above 200 µg/mL. Therefore, the molecule mixture of the BPF aims to ensure good performance of the mitochondrial bioenergetic parameters. Full article
(This article belongs to the Special Issue Recent Advances in Metabolism and Oxidative Stress in Human Diseases)
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Review

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18 pages, 1607 KiB  
Review
The Biological Relevance of Papaverine in Cancer Cells
by Daniella Anthea Gomes, Anna Margaretha Joubert and Michelle Helen Visagie
Cells 2022, 11(21), 3385; https://doi.org/10.3390/cells11213385 - 26 Oct 2022
Cited by 6 | Viewed by 2492
Abstract
Papaverine (PPV), a benzylisoquinoline alkaloid, extracted from the Papaverine somniferum plant, is currently in clinical use as a vasodilator. Research has shown that PPV inhibits phosphodiesterase 10A (PDE10A,) resulting in the accumulation of cyclic adenosine 3′, 5′-monophosphate (cAMP) that affects multiple downstream pathways, [...] Read more.
Papaverine (PPV), a benzylisoquinoline alkaloid, extracted from the Papaverine somniferum plant, is currently in clinical use as a vasodilator. Research has shown that PPV inhibits phosphodiesterase 10A (PDE10A,) resulting in the accumulation of cyclic adenosine 3′, 5′-monophosphate (cAMP) that affects multiple downstream pathways, including phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt), a mammalian target of rapamycin (mTOR) and vascular endothelial growth factor (VEGF). The accumulation of cAMP can further affect mitochondrial metabolism through the activation of protein kinase A (PKA), which activates the mitochondrial complex I. Literature has shown that PPV exerts anti-proliferative affects in several tumorigenic cell lines including adenocarcinoma alveolar cancer (A549) and human hepatoma (HepG-2) cell lines. Cell cycle investigations have shown varying results with the effects dependent on concentration and cell type with data suggesting an increase in cells occupying the sub-G1 phase, which is indicative of cell death. These results suggest that PPV may be a beneficial compound to explore for the use in anticancer studies. More insight into the effects of the compound on cellular and molecular mechanisms is needed. Understanding the effects PPV may exert on tumorigenic cells may better researchers’ understanding of phytomedicines and the effects of PPV and PPV-derived compounds in cancer. Full article
(This article belongs to the Special Issue Recent Advances in Metabolism and Oxidative Stress in Human Diseases)
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27 pages, 1648 KiB  
Review
Effects of Noonan Syndrome-Germline Mutations on Mitochondria and Energy Metabolism
by Donald Bajia, Emanuela Bottani and Katarzyna Derwich
Cells 2022, 11(19), 3099; https://doi.org/10.3390/cells11193099 - 1 Oct 2022
Cited by 6 | Viewed by 3740
Abstract
Noonan syndrome (NS) and related Noonan syndrome with multiple lentigines (NSML) contribute to the pathogenesis of human diseases in the RASopathy family. This family of genetic disorders constitute one of the largest groups of developmental disorders with variable penetrance and severity, associated with [...] Read more.
Noonan syndrome (NS) and related Noonan syndrome with multiple lentigines (NSML) contribute to the pathogenesis of human diseases in the RASopathy family. This family of genetic disorders constitute one of the largest groups of developmental disorders with variable penetrance and severity, associated with distinctive congenital disabilities, including facial features, cardiopathies, growth and skeletal abnormalities, developmental delay/mental retardation, and tumor predisposition. NS was first clinically described decades ago, and several genes have since been identified, providing a molecular foundation to understand their physiopathology and identify targets for therapeutic strategies. These genes encode proteins that participate in, or regulate, RAS/MAPK signalling. The RAS pathway regulates cellular metabolism by controlling mitochondrial homeostasis, dynamics, and energy production; however, little is known about the role of mitochondrial metabolism in NS and NSML. This manuscript comprehensively reviews the most frequently mutated genes responsible for NS and NSML, covering their role in the current knowledge of cellular signalling pathways, and focuses on the pathophysiological outcomes on mitochondria and energy metabolism. Full article
(This article belongs to the Special Issue Recent Advances in Metabolism and Oxidative Stress in Human Diseases)
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Other

12 pages, 3116 KiB  
Perspective
Platelet Metabolic Flexibility: A Matter of Substrate and Location
by Silvia Ravera, Maria Grazia Signorello and Isabella Panfoli
Cells 2023, 12(13), 1802; https://doi.org/10.3390/cells12131802 - 7 Jul 2023
Cited by 2 | Viewed by 1335
Abstract
Platelets are cellular elements that are physiologically involved in hemostasis, inflammation, thrombotic events, and various human diseases. There is a link between the activation of platelets and their metabolism. Platelets possess considerable metabolic versatility. Although the role of platelets in hemostasis and inflammation [...] Read more.
Platelets are cellular elements that are physiologically involved in hemostasis, inflammation, thrombotic events, and various human diseases. There is a link between the activation of platelets and their metabolism. Platelets possess considerable metabolic versatility. Although the role of platelets in hemostasis and inflammation is known, our current understanding of platelet metabolism in terms of substrate preference is limited. Platelet activation triggers an oxidative metabolism increase to sustain energy requirements better than aerobic glycolysis alone. In addition, platelets possess extra-mitochondrial oxidative phosphorylation, which could be one of the sources of chemical energy required for platelet activation. This review aims to provide an overview of flexible platelet metabolism, focusing on the role of metabolic compartmentalization in substrate preference, since the metabolic flexibility of stimulated platelets could depend on subcellular localization and functional timing. Thus, developing a detailed understanding of the link between platelet activation and metabolic changes is crucial for improving human health. Full article
(This article belongs to the Special Issue Recent Advances in Metabolism and Oxidative Stress in Human Diseases)
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