Mitochondrial dysfunction in aging: Much progress but many unresolved questions
Open accessAbstract
The free radical theory of aging is almost 60 years old. As mitochondria are the principle source of intracellular reactive oxygen species (ROS), this hypothesis suggested a central role for the mitochondrion in normal mammalian aging. In recent years, however, much work has questioned the importance of mitochondrial ROS in driving aging. Conversely new evidence points to other facets of mitochondrial dysfunction which may nevertheless suggest the mitochondrion retains a critical role at the center of a complex web of processes leading to cellular and organismal aging.
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Mitochondrial dysfunction is a major contributor to aging and aging-driven degenerative diseases such as diabetes, heart diseases, cancer, Alzheimer's disease and Parkinson's disease.
“It is now recognized that mitochondrial dysfunction is a major contributor to aging and aging-driven degenerative disease, such as diabetes, heart diseases, cancer, Alzheimer’s disease and Parkinson’s disease [35,36,37,38,39,40].”
From The mitochondrial permeability transition: Nexus of aging, disease and longevity (2021) · cites this paper as [36]
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References 108 · Cited by 335
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- [69]Short K.R. Bigelow M.L. Kahl J. Singh R. Coenen-Schimke J. Raghavakaimal S. Nair K.S. Decline in skeletal muscle mitochondrial function with aging in humans Proc. Natl. Acad. Sci. U. S. A. 102 2005 5618 5623 15800038 PMC556267
- [75]Conley K.E. Jubrias S.A. Esselman P.C. Oxidative capacity and ageing in human muscle J. Physiol. 526 2000 203 210 10878112 PMC2269983
- Authors
- Payne, B. A. I., & Chinnery, P. F.
- Affiliations
- Wellcome Centre for Mitochondrial Research (GB)
- Corresponding author
- Chinnery, Patrick F.
- Venue
- Biochimica et Biophysica Acta (BBA) - Bioenergetics
- Publisher
- Elsevier BV
- Published
- 2015-11
- Volume
- 1847
- Issue
- 11
- Pages
- 1347-1353
- ISSN
- 0005-2728 (ISSN-L)
- PMC
- PMC4580208
- OpenAlex
- W604196653
- Cited by
- 335
- References
- 108
- Citations by year
- 2026: 12 · 2025: 18 · 2024: 29 · 2023: 23 · 2022: 26 · 2021: 37 · 2020: 34 · 2019: 34 · 2018: 58 · 2017: 31 · 2016: 27 · 2015: 6
- FWCI
- 17.64
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Biochimica et Biophysica Acta (BBA) - Bioenergetics (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Newcastle University ePrints (Newcastle Univesity) (cc-by)
- Funders
- Academy of Medical Sciences
- The Wellcome Trust
- Medical Research Council
- British Heart Foundation
- Arthritis Research UK
- Prostate Cancer UK
- Royal College of Physicians
- Wellcome Trust (101876/Z/13/Z, 096919Z/11/Z)
- Medical Research Council (UK) Centre for Translational Muscle Disease research (G0601943, EU FP7 TIRCON)
- National Institute for Health Research (NIHR)
- Newcastle Biomedical Research Centre
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial dysfunction, aging, free radical theory of aging, reactive oxygen species, mitochondrial reactive oxygen species, cellular aging, biological aging
- MeSH terms
- Aging, Animals, DNA, Mitochondrial, Humans, Mitochondria, Mutation, Reactive Oxygen Species, Mitochondrial Proton-Translocating ATPases
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