Dietary restriction.; mitochondrial function and aging: From yeast to humans
Open accessAbstract
Dietary restriction (DR) attenuates many detrimental effects of aging and consequently promotes health and increases longevity across organisms. While over the last 15 years extensive research has been devoted towards understanding the biology of aging, the precise mechanistic aspects of DR are yet to be settled. Abundant experimental evidence indicates that the DR effect on stimulating health impinges several metabolic and stress-resistance pathways. Downstream effects of these pathways include a reduction in cellular damage induced by oxidative stress, enhanced efficiency of mitochondrial functions and maintenance of mitochondrial dynamics and quality control, thereby attenuating age-related declines in mitochondrial function. However, the literature also accumulates conflicting evidence regarding how DR ameliorates mitochondrial performance and whether that is enough to slow age-dependent cellular and organismal deterioration. Here, we will summarize the current knowledge about how and to which extent the influence of different DR regimes on mitochondrial biogenesis and function contribute to postpone the detrimental effects of aging on health-span and lifespan. This article is part of a Special Issue entitled: Mitochondrial Dysfunction in Aging.
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Dietary restrictions increase lifespan and healthspan in all animal models of aging (yeast, C. elegans, Drosophila, mouse).
“Dietary restrictions have been shown to increase lifespan and healthspan in all animal models of aging (e.g., yeast, C. elegans, Drosophila, mouse) [239,289,290,291].”
From The mitochondrial permeability transition: Nexus of aging, disease and longevity (2021) · cites this paper as [290]
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References 157 · Cited by 139
Research works printed but not linked: 1
- [154]Colman RJ Beasley TM Kemnitz JW Johnson SC Weindruch R Anderson RM Caloric restriction reduces age-related and all-cause mortality in rhesus monkeys Nat Commun 2014 5 3557 10.1038/ncomms4557 24691430 PMC3988801 · DOI · Paper page
- Authors
- Ruetenik, A., & Barrientos, A.
- Affiliations
- University of Miami (US)
- Corresponding author
- Barrientos, Antoni
- ORCID
- Barrientos, Antoni
- Venue
- Biochimica et Biophysica Acta (BBA) - Bioenergetics
- Publisher
- Elsevier BV
- Published
- 2015-11
- Volume
- 1847
- Issue
- 11
- Pages
- 1434-1447
- ISSN
- 0005-2728 (ISSN-L)
- PMC
- PMC4575837
- OpenAlex
- W2172781613
- Cited by
- 139
- References
- 157
- Citations by year
- 2026: 8 · 2025: 7 · 2024: 7 · 2023: 6 · 2022: 15 · 2021: 12 · 2020: 16 · 2019: 16 · 2018: 22 · 2017: 14 · 2016: 12 · 2015: 4
- FWCI
- 1.52
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Bioenergetics (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of General Medical Sciences (GM112179, GM105781, R01GM071775, R01GM112179, R01GM105781)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- dietary restriction, aging, mitochondrial function, mitochondrial biogenesis, mitochondrial dynamics, mitochondrial quality control, oxidative stress, longevity, healthspan, lifespan, stress tolerance
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Mechanistic Target of Rapamycin Complex 1, Adenylate Kinase, Aging, Humans, Longevity, Mitochondria, Saccharomyces cerevisiae, Transcription Factors, Signal Transduction, Caloric Restriction, Sirtuins, Multiprotein Complexes, TOR Serine-Threonine Kinases
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