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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 3409

Special Issue Editor


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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
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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

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Keywords

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

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Published Papers (2 papers)

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Research

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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
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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
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Review

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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
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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
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