ArticleProceedings of the National Academy of Sciences of the United States of America2020
Moderation of mitochondrial respiration mitigates metabolic syndrome of aging.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 64 citations in OpenAlex.
- Predicting and finding geroprotective compounds through modulating conserved longevity-associated aging modules.Science advances · 2026Article
- Mitochondrial Enzymes Mimetic Ultrasmall Palladium Nanozymes Prevent Senescence and Neurodegeneration Through Metabolic Reprogramming.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- TPP-Thiazole Derivatives Ameliorate Psoriasiform Inflammation by Glycolysis Inhibition.Molecules (Basel, Switzerland) · 2026Article
- Effect of prolonged voluntary wheel running on oxidative stress and defence mechanisms in cortex and hippocampus of healthy female rats.Experimental physiology · 2026Article
- Regulation of Mitochondrial Homeostasis: Applications of Nanobiomaterials in Age-Related Bone Diseases.International journal of nanomedicine · 2026Review
- Immunosenescence in aging and neurodegenerative diseases: evidence, key hallmarks, and therapeutic implications.Translational neurodegeneration · 2025Review
- Age-related changes in the proteome and mitochondrial metabolism of rabbit adipose-derived stromal/stem cells.Scientific reports · 2025Article
- Young small extracellular vesicles rejuvenate replicative senescence by remodeling Drp1 translocation-mediated mitochondrial dynamics.Journal of nanobiotechnology · 2024Article
- Markers of Mitochondrial Function and DNA Repair Associated with Physical Function in Centenarians.Biomolecules · 2024Article
- Application Prospects of Triphenylphosphine-Based Mitochondria-Targeted Cancer Therapy.Cancers · 2023Review
- The role of cellular senescence in metabolic diseases and the potential for senotherapeutic interventions.Frontiers in cell and developmental biology · 2023Review
- Naked mole-rat and Damaraland mole-rat exhibit lower respiration in mitochondria, cellular and organismal levels.Biochimica et biophysica acta. Bioenergetics · 2022Article
- Antagonistic effects of mitochondrial matrix and intermembrane space proteases on yeast aging.BMC biology · 2022Article
- Article
- Neutral Sphingomyelinase 2 Mediates Oxidative Stress Effects on Astrocyte Senescence and Synaptic Plasticity Transcripts.Molecular neurobiology · 2022Article
- Mitochondrial and metabolic dysfunction in ageing and age-related diseases.Nature reviews. Endocrinology · 2022Review
- Metformin, phenformin, and galegine inhibit complex IV activity and reduce glycerol-derived gluconeogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Maintenance of Chronological Aging Features in Culture of Normal Human Dermal Fibroblasts from Old Donors.Cells · 2022Article
- Molecular markers of DNA repair and brain metabolism correlate with cognition in centenarians.GeroScience · 2022Article
- The Role of Mitochondrial Quality Control in Anthracycline-Induced Cardiotoxicity: From Bench to Bedside.Oxidative medicine and cellular longevity · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deregulation of mitochondrial dynamics leads to the accumulation of oxidative stress and unhealthy mitochondria; consequently, this accumulation contributes to premature aging and alterations in mitochondria linked to metabolic complications. We postulate that restrained mitochondrial ATP synthesis might alleviate age-associated disorders and extend healthspan in mammals. Herein, we prepared a previously discovered mitochondrial complex IV moderate inhibitor in drinking water and orally administered to standard-diet-fed, wild-type C57BL/6J mice every day for up to 16 mo. No manifestation of any apparent toxicity or deleterious effect on studied mouse models was observed. The impacts of an added inhibitor on a variety of mitochondrial functions were analyzed, such as respiratory activity, mitochondrial bioenergetics, and biogenesis, and a few age-associated comorbidities, including reactive oxygen species (ROS) production, glucose abnormalities, and obesity in mice. It was found that mitochondrial quality, dynamics, and oxidative metabolism were greatly improved, resulting in lean mice with a specific reduction in visceral fat plus superb energy and glucose homeostasis during their aging period compared to the control group. These results strongly suggest that a mild interference in ATP synthesis through moderation of mitochondrial activity could effectively up-regulate mitogenesis, reduce ROS production, and preserve mitochondrial integrity, thereby impeding the onset of metabolic syndrome. We conclude that this inhibitory intervention in mitochondrial respiration rectified the age-related physiological breakdown in mice by protecting mitochondrial function and markedly mitigated certain undesired primary outcomes of metabolic syndrome, such as obesity and type 2 diabetes. This intervention warrants further research on the treatment of metabolic syndrome of aging in humans.
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