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Mitochondrial biogenesis and healthy aging
Open accessAbstract
Aging is associated with an overall loss of function at the level of the whole organism that has origins in cellular deterioration. Most cellular components, including mitochondria, require continuous recycling and regeneration throughout the lifespan. Mitochondria are particularly susceptive to damage over time as they are the major bioenergetic machinery and source of oxidative stress in cells. Effective control of mitochondrial biogenesis and turnover, therefore, becomes critical for the maintenance of energy production, the prevention of endogenous oxidative stress and the promotion of healthy aging. Multiple endogenous and exogenous factors regulate mitochondrial biogenesis through the peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha). Activators of PGC-1alpha include nitric oxide, CREB and AMPK. Calorie restriction (CR) and resveratrol, a proposed CR mimetic, also increase mitochondrial biogenesis through activation of PGC-1alpha. Moderate exercise also mimics CR by inducing mitochondrial biogenesis. Negative regulators of PGC-1alpha such as RIP140 and 160MBP suppress mitochondrial biogenesis. Another mechanism involved in mitochondrial maintenance is mitochondrial fission/fusion and this process also involves an increasing number of regulatory proteins. Dysfunction of either biogenesis or fission/fusion of mitochondria is associated with diseases of the neuromuscular system and aging, and a greater understanding of the regulation of these processes should help us to ultimately control the aging process.
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“rRenovation of the mitochondrial network plays a key role in health-span increase after CR (Lopez-Lluch et al., 2008)”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Lopez-Lluch et al., 2008
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Metadata
- Authors
- López-Lluch, G., Irusta, P. M., Navas, P., & de Cabo, R.
- Affiliations
- Georgetown University (US)
- Venue
- Experimental Gerontology
- Publisher
- Elsevier BV
- Published
- 2008-09
- Volume
- 43
- Issue
- 9
- Pages
- 813-819
- ISSN
- 0531-5565 (ISSN-L)
- PMC
- PMC2562606
- OpenAlex
- W2007256995
- Cited by
- 364
- References
- 85
- Citations by year
- 2026: 13 · 2025: 10 · 2024: 14 · 2023: 15 · 2022: 20 · 2021: 17 · 2020: 16 · 2019: 21 · 2018: 17 · 2017: 19 · 2016: 16 · 2015: 30 · 2014: 16 · 2013: 31 · 2012: 26
- FWCI
- 2.13
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Experimental Gerontology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (Z01AG000368)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial biogenesis, healthy aging, PGC-1α, oxidative stress, caloric restriction, resveratrol, AMPK, CREB, nitric oxide, RIP140, mitochondrial fission and fusion, physical activity, mitochondrial turnover, neuromuscular disorders
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Aging, Animals, Heat-Shock Proteins, Hormones, Humans, Mitochondria, Transcription Factors, Neurodegenerative Diseases, Caloric Restriction
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