ijms-logo

Journal Browser

Journal Browser

Cell Metabolism: Its Physiology, Dysfunction, and Related Metabolic Complications

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 January 2025 | Viewed by 4044

Special Issue Editor


E-Mail Website
Guest Editor
Department of Biological Sciences, Ulsan National Institute of Science and Technology, Ulsan 44919, Republic of Korea
Interests: DNA methylation; TET proteins; hematopoietic stem cells; hematopoiesis; leukemia; cancer epigenetics; cancer therapy; drug screen; metabolic diseases; obesity; diabetes; biosensor; signaling and gene expression
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolism, the cornerstone of life, is finely orchestrated by the complex interplay among cells within specialized tissues, notably adipocytes, muscle cells, and hepatocytes. Adipocytes govern systemic energy and glucose homeostasis, thermogenesis, and hormone secretion. Muscle cells, with their high energy demands, also play a central role in glucose uptake and utilization. Dysfunction within these cells disrupts the metabolic balance, contributing to various complications, including insulin resistance, obesity, diabetes, and cardiovascular diseases. Additionally, hepatocytes, the metabolic powerhouses, also dictate glucose and lipid metabolism and detoxification, and they are the central players in diabetes, fatty liver disease, hepatic inflammation and fibrosis, and liver cancers. This Special Issue aims to explore the intricate molecular events and mechanisms that underlie both normal and aberrant cellular metabolism, along with the associated metabolic disorders.

We invite submissions of original research articles, reviews, and clinical studies that address, but are not limited to, the following areas:

  • Molecular insights into adipocyte differentiation and function;
  • Adipose tissue inflammation and metabolic dysfunction;
  • Role of adipokines in metabolism;
  • Adipose tissue remodeling in health and disease;
  • Hepatic glucose and lipid metabolism;
  • Crosstalk among liver, muscle, and adipose tissues in metabolic regulation;
  • Genetic and epigenetic regulation of metabolism;
  • Obesity and diabetes: mechanisms, complications, and therapeutic interventions;
  • Steatosis, hepatitis, and cirrhosis: underlying mechanisms and therapeutic targets;
  • Liver cancers: pathology and therapeutic strategies;
  • Innovative therapeutic approaches to treat metabolic diseases.

We look forward to receiving your contributions.

Dr. Myunggon Ko
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.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • cell metabolism
  • adipocytes
  • muscle cells
  • hepatocytes
  • insulin resistance
  • inflammation
  • obesity
  • diabetes
  • hepatic disorders
  • cardiovascular diseases
  • cancers

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

13 pages, 2220 KiB  
Article
Oligonol®, an Oligomerized Polyphenol from Litchi chinensis, Enhances Branched-Chain Amino Acid Transportation and Catabolism to Alleviate Sarcopenia
by Yun-Ching Chang, Yu-Chi Chen, Yin-Ching Chan, Cheng Liu and Sue-Joan Chang
Int. J. Mol. Sci. 2024, 25(21), 11549; https://doi.org/10.3390/ijms252111549 - 27 Oct 2024
Viewed by 1157
Abstract
Branched-chain amino acids (BCAAs) are essential for muscle protein synthesis and are widely acknowledged for mitigating sarcopenia. Oligonol® (Olg), a low-molecular-weight polyphenol from Litchi chinensis, has also been found to attenuate sarcopenia by improving mitochondrial quality and positive protein turnover. This [...] Read more.
Branched-chain amino acids (BCAAs) are essential for muscle protein synthesis and are widely acknowledged for mitigating sarcopenia. Oligonol® (Olg), a low-molecular-weight polyphenol from Litchi chinensis, has also been found to attenuate sarcopenia by improving mitochondrial quality and positive protein turnover. This study aims to investigate the effect of Olg on BCAA-stimulated protein synthesis in sarcopenia. In sarcopenic C57BL/6 mice and senescence-accelerated mouse-prone 8 (SAMP8) mice, BCAAs were significantly decreased in skeletal muscle but increased in blood serum. Furthermore, the expressions of membrane L-type amino acid transporter 1 (LAT1) and branched-chain amino acid transaminase 2 (BCAT2) in skeletal muscle were lower in aged mice than in young mice. The administration of Olg for 8 weeks significantly increased the expressions of membrane LAT1 and BCAT2 in the skeletal muscle when compared with non-treated SAMP8 mice. We further found that BCAA deprivation via LAT1-siRNA in C2C12 myotubes inhibited the signaling of protein synthesis and facilitated ubiquitination degradation of BCAT2. In C2C12 cells mimicking sarcopenia, Olg combined with BCAA supplementation enhanced mTOR/p70S6K activity more than BCAA alone. However, blocked LAT1 by JPH203 reversed the synergistic effect of the combination of Olg and BCAAs. Taken together, changes in LAT1 and BCAT2 during aging profoundly alter BCAA availability and nutrient signaling in aged mice. Olg increases BCAA-stimulated protein synthesis via modulating BCAA transportation and BCAA catabolism. Combining Olg and BCAAs may be a useful nutritional strategy for alleviating sarcopenia. Full article
Show Figures

Figure 1

Review

Jump to: Research

23 pages, 2243 KiB  
Review
Combining Photodynamic Therapy and Targeted Drug Delivery Systems: Enhancing Mitochondrial Toxicity for Improved Cancer Outcomes
by J. P. Jose Merlin, Anine Crous and Heidi Abrahamse
Int. J. Mol. Sci. 2024, 25(19), 10796; https://doi.org/10.3390/ijms251910796 - 8 Oct 2024
Viewed by 2106
Abstract
Cancer treatment continues to be a substantial problem due to tumor complexities and persistence, demanding novel therapeutic techniques. This review investigates the synergistic potential of combining photodynamic therapy (PDT) and tailored medication delivery technologies to increase mitochondrial toxicity and improve cancer outcomes. PDT [...] Read more.
Cancer treatment continues to be a substantial problem due to tumor complexities and persistence, demanding novel therapeutic techniques. This review investigates the synergistic potential of combining photodynamic therapy (PDT) and tailored medication delivery technologies to increase mitochondrial toxicity and improve cancer outcomes. PDT induces selective cellular damage and death by activating photosensitizers (PS) with certain wavelengths of light. However, PDT’s efficacy can be hampered by issues such as poor light penetration and a lack of selectivity. To overcome these challenges, targeted drug delivery systems have emerged as a promising technique for precisely delivering therapeutic medicines to tumor cells while avoiding off-target effects. We investigate how these technologies can improve mitochondrial targeting and damage, which is critical for causing cancer cell death. The combination method seeks to capitalize on the advantages of both modalities: selective PDT activation and specific targeted drug delivery. We review current preclinical and clinical evidence supporting the efficacy of this combination therapy, focusing on case studies and experimental models. This review also addresses issues such as safety, distribution efficiency, resistance mechanisms, and costs. The prospects of further research include advances in photodynamic agents and medication delivery technology, with a focus on personalized treatment. In conclusion, combining PDT with targeted drug delivery systems provides a promising frontier in cancer therapy, with the ability to overcome current treatment limits and open the way for more effective, personalized cancer treatments. Full article
Show Figures

Figure 1

Back to TopTop