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Nutrient Interaction, Metabolic Adaptation and Healthy Aging

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Geriatric Nutrition".

Deadline for manuscript submissions: 25 January 2026 | Viewed by 462

Special Issue Editors


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Guest Editor
National Institute for Nutrition and Health, Chinese Center for Disease Control and Prevention, Beijing 100050, China
Interests: animal experiments on the pathogenesis of diseases (e.g., nutrients, interactions, metabolic reprogramming, mechanisms)

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Guest Editor
School of Public Health, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China
Interests: population epidemiology and cohort studies (e.g., nutritional epidemiology, metabolic dysfunction-associated steatotic liver disease, type 2 diabetes, cardiovascular disease)
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Special Issue Information

Dear Colleagues,

Aging is a complex and multifactorial process that is determined by many factors, including genetic background, metabolic regulation, and external environmental factors. Unhealthy aging is a major risk factor for the development of many diseases, prominently including neurodegenerative disease, cancer, diabetes, and cardiovascular disease. In the central nervous system, microglia can quickly adapt to varying nutrient availability, transitioning from glycolysis to other metabolic pathways such as glutaminolysis under acute stress. Under neuroinflammatory conditions, metabolic reprogramming occurs primarily through a shift from oxidative glycolysis to aerobic glycolysis, essential for proper cytokine release. In tumorigenesis, beyond the metabolic reprogramming of the glucose metabolism, the important role of other amino acids, such as serine, glycine, and methionine, gradually becomes clear. Diabetic neuropathy is often a formidable challenge in the clinical management of diabetes, markedly diminishing the patient's quality of life, and is now liked to toxic sphingolipids caused by metabolic reprogramming due to serine deficiency. Other nutrients, such as elenium and vitamin K, have recently become to be considered as key regulators of ferroptosis—which is a newly identified novel form of regulated, non-apoptotic cell death caused by iron-overload-dependent phospholipid peroxidation—and then influences cell aging, tumorigenesis, and cell death.

We welcome original in vitro, animal, and human studies, as well as reviews of the scholarship around aging. Submissions that address the mechanisms of genetic and epigenetic adaptation and metabolic programming among metabolic pathways, the interactions of nutrients during healthy aging, as well as nutrient imbalance under disease conditions and nutrient rebalancing for disease prevention and treatment are strongly encouraged.

In this Special Issue, we focus on high-quality studies on the interactions and rebalancing of nutrients that benefit healthy aging.

Dr. Zhenwu Huang
Dr. Shunming Zhang
Guest Editors

Manuscript Submission Information

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Keywords

  • nutrients
  • healthy aging
  • genetic and epigenetic mechanisms
  • metabolic reprogramming
  • interaction
  • intervention

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Published Papers (1 paper)

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Research

17 pages, 3096 KB  
Article
Activation of Sirtuin3 by 6,4′-Dihydroxy-7-methoxyflavanone Against Myoblasts Senescence by Attenuating D-Galactose-Induced Oxidative Stress and Inflammation
by Bingsi Li, Yuxuan Gu, Libing Zhou, Rui Chen, Yiwei Liu, Zexuan Wan, Ziyi Liang, Yukang Wang, Renlei Ji and Zhian Liu
Nutrients 2025, 17(20), 3298; https://doi.org/10.3390/nu17203298 - 20 Oct 2025
Viewed by 333
Abstract
Background/Objective: Cellular senescence is increasingly recognized as a key mechanism underlying sarcopenia, an age-related muscle disorder with no effective therapeutic. 6,4′-Dihydroxy-7-methoxyflavanone (DMF), a flavonoid isolated from Dalbergia odorifera T. Chen, has shown anti-senescence potential. This study aimed to investigate the protective effects of [...] Read more.
Background/Objective: Cellular senescence is increasingly recognized as a key mechanism underlying sarcopenia, an age-related muscle disorder with no effective therapeutic. 6,4′-Dihydroxy-7-methoxyflavanone (DMF), a flavonoid isolated from Dalbergia odorifera T. Chen, has shown anti-senescence potential. This study aimed to investigate the protective effects of DMF against myoblasts senescence and elucidate the underlying molecular mechanisms. Method: A cellular model of senescence was established in C2C12 myoblasts using D-galactose (D-gal). The effects of DMF pretreatment were evaluated by assessing senescence phenotypes, myogenic differentiation, and mitochondrial function. The role of Sirtuin3 (SIRT3) was confirmed using siRNA-mediated knockdown. Results: DMF Pre-treatment effectively attenuated D-gal-induced senescence, as indicated by restored proliferation, reduced senescence-associated β-galactosidase activity, decreased DNA damage, and the downregulation of p53, p21Cip1/WAF1 and p16INK4a. Furthermore, DMF rescued myogenic differentiation capacity, enhancing the expression of Myoblast determination protein 1, Myogenin, Myosin heavy chain and Muscle-specific regulatory factor 4, and promoting myotube formation. Mechanistically, DMF was identified as a SIRT3 activator. It enhanced SIRT3 expression and activity, leading to the deacetylation and activation of the mitochondrial antioxidant enzyme superoxide dismutase 2. This consequently reduced mitochondrial reactive oxygen species, improved mitochondrial membrane potential and ATP production, and suppressed the NF-κB pathway by inhibiting IκBα phosphorylation and p65 acetylation/nuclear translocation. Crucially, all the beneficial effects of DMF—including oxidative stress reduction, mitochondrial functional recovery, anti-inflammatory action, and ultimately, the attenuation of senescence and improvement of myogenesis—were abolished upon SIRT3 knockdown. Conclusions: Our findings demonstrate that DMF alleviates myoblasts senescence and promotes myogenic differentiation by activating the SIRT3-SOD2 pathway, thereby reducing oxidative stress and NF-κB-driven inflammation responses. DMF emerges as a promising therapeutic candidate for sarcopenia. Full article
(This article belongs to the Special Issue Nutrient Interaction, Metabolic Adaptation and Healthy Aging)
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