The role of mitochondrial dysfunction in age-related diseases
Open accessAbstract
The aging process is accompanied by the onset of disease and a general decline in wellness. Insights into the aging process have revealed a number of cellular hallmarks of aging, among these epigenetic alterations, loss of proteostasis, mitochondrial dysfunction, cellular senescence, and stem cell exhaustion. Mitochondrial dysfunction increasingly appears to be a common factor connecting several of these hallmarks, driving the aging process and afflicting tissues throughout the body. Recent research has uncovered a much more complex involvement of mitochondria in the cell than has previously been appreciated and revealed novel ways in which mitochondrial defects feed into disease pathology. In this review we evaluate ways in which problems in mitochondria contribute to disease beyond the well-known mechanisms of oxidative stress and bioenergetic deficits, and we predict the direction that mitochondrial disease research will take in years to come.
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Mitochondrial dysfunction has been associated with age-related diseases such as neurological disorders, cardiovascular disease, liver and kidney diseases, diabetes and cancer.
“it has been associated with a number of age-related diseases such as neurological disorders, cardiovascularCVD, liver and kidney diseases, diabetes and cancer (Lane et al., 2015; Payne and Chinnery, 2015; Ryan et al., 2015; Wallace, 2012).”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Lane et al., 2015
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 [35]
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- Authors
- Lane, R. K., Hilsabeck, T., & Rea, S. L.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Corresponding author
- Rea, Shane L.
- Venue
- Biochimica et Biophysica Acta (BBA) - Bioenergetics
- Publisher
- Elsevier BV
- Published
- 2015-11
- Volume
- 1847
- Issue
- 11
- Pages
- 1387-1400
- ISSN
- 0005-2728 (ISSN-L)
- PMC
- PMC10481969
- OpenAlex
- W625172625
- Cited by
- 205
- References
- 200
- Citations by year
- 2026: 7 · 2025: 15 · 2024: 15 · 2023: 16 · 2022: 22 · 2021: 25 · 2020: 27 · 2019: 20 · 2018: 12 · 2017: 21 · 2016: 22 · 2015: 3
- FWCI
- 1.87
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Bioenergetics (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute for Aging
- R21AG047561 (SLR)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- mitochondrial dysfunction, aging, age-related diseases, cellular senescence, stem cell exhaustion, proteostasis, epigenetic modifications, oxidative stress, mitochondrial disease
- MeSH terms
- Aging, Animals, Cell Differentiation, Humans, Mitochondria, Osteoporosis, Stem Cells, Neurodegenerative Diseases, Atherosclerosis
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