Influence of aging on membrane permeability transition in brain mitochondria
Open accessAbstract
The mitochondrial inner membrane permeability transition (MPT) plays an important role in the pathophysiology of acute disorders of the central nervous systems, including ischemic and traumatic brain injury, and possibly in neurodegenerative diseases. Opening of the permeability transition pore (PTP) by a combination of abnormally elevated intramitochondrial Ca2+ and oxidative stress induces the collapse of transmembrane ion gradients, resulting in membrane depolarization and uncoupling of oxidative phosphorylation. This loss of ATP synthesis eventually results in cellular metabolic failure and necrotic cell death. Drugs, e.g., cyclosporin A, can inhibit the permeability transition through their interaction with the mitochondria-specific protein, cyclophilin D, and demonstrate neuroprotection in several animal models. These characteristics of the MPT were developed almost exclusively from experiments performed with young, mature rodents whereas the neuropathologies associated with the MPT are most prevalent in the elderly population. Some evidence indicates that the sensitivity of mitochondria to Ca2+-induced PTP opening is greater in the aged compared to the young mature brain; however, the basis for this difference is unknown. Based on knowledge of factors that regulate the MPT and on other comparisons between cells and mitochondria from young and old animals, several features may be important. These aging-related features include impaired neuronal Ca2+ homeostasis, increased oxidative stress, increased cyclophilin D protein levels, oxidative modification of the adenine nucleotide translocase and of cardiolipin, and changes in the levels of anti-death mitochondrial proteins, e.g., Bcl-2. The influence of aging on both the contribution of the MPT to neuropathology and the neuroprotective efficacy of MPT inhibitors is a substantial knowledge gap that requires extensive research at the subcellular, cellular, and animal model levels.
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Direct evidence for enhanced mPTP activation in aging and neurodegenerative disease is extensive.
“Indeed, direct evidence for enhanced mPTP activation in aging and neurodegenerative disease is extensive.”
From The mitochondrial permeability transition: Nexus of aging, disease and longevity (2021) · cites this paper as [43]
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- Authors
- Toman, J., & Fiskum, G.
- Affiliations
- University of Maryland, Baltimore (US)
- Corresponding author
- Fiskum, Gary
- Venue
- Journal of Bioenergetics and Biomembranes
- Published
- 2011-02
- Volume
- 43
- Issue
- 1
- Pages
- 3-10
- ISSN
- 0145-479X (ISSN-L)
- 1573-6881
- PMC
- PMC4085790
- OpenAlex
- W2074049363
- Cited by
- 69
- References
- 59
- Citations by year
- 2025: 1 · 2024: 2 · 2023: 2 · 2022: 2 · 2021: 5 · 2020: 3 · 2019: 4 · 2018: 5 · 2017: 8 · 2016: 7 · 2015: 6 · 2014: 3 · 2013: 9 · 2012: 6
- FWCI
- 0.70
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Journal of Bioenergetics and Biomembranes (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (T35AG036679)
- National Institute of Neurological Disorders and Stroke (R01NS034152)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (P01HD016596)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
- Keywords
- mitochondrial permeability transition, brain mitochondria, aging, mitochondrial permeability transition pore, cyclophilin D, cyclosporine, mitochondrial calcium, oxidative stress, neuronal calcium homeostasis, adenine nucleotide translocase, cardiolipin oxidation, Bcl-2, mitochondrial depolarization, mitochondrial uncoupling, neuroprotection, neurodegenerative diseases, ischemic brain injury, traumatic brain injury
- MeSH terms
- Mitochondrial Permeability Transition Pore, Aging, Animals, Brain, Calcium, Humans, Permeability, Oxidative Stress, Neurodegenerative Diseases, Mitochondrial Membrane Transport Proteins, Mitochondrial Membranes
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