Mitochondrial function and myocardial aging. A critical analysis of the role of permeability transition
Open accessAbstract
Mitochondria have been suggested to be causally linked to age-related alterations through respiratory chain dysfunction and formation of reactive oxygen species, leading to damage of mitochondrial DNA. Impaired biosynthesis of respiratory chain and ATP synthase subunits encoded by mitochondrial genes would set up a vicious cycle contributing to the aging process. Mitochondria are also involved in the increased susceptibility to ischemic injury observed in aged hearts, a process where the mitochondrial permeability transition pore (PTP) may play a role. Here, we analyze (i) the possible mechanisms through which PTP opening might contribute to age-related myocardial alterations; (ii) the available evidence of an increased probability of PTP opening in mitochondria isolated from aged tissues; (iii) the current methodological limitations that complicate the elucidation of causal relationships between PTP opening, mitochondrial dysfunction, and myocardial aging.
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Alterations in redox status and impairment in oxidative phosphorylation sensitize mitochondria in older adults to permeability transition pore opening, leading to cellular energetic failure and necrotic or programmed cell death in cardiomyocytes or other tissue.
“Alterations in redox status and impairment in oxidative phosphorylation also sensitize mitochondria in older adults to permeability transition pore opening that in turn leads to cellular energetic failure and necrotic or programmed cell death in cardiomyocytes or other tissue.30”
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 [42]
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References 147 · Cited by 139
Research works printed but not linked: 3
- Szibor M, Holtz J. Mitochondrial ageing. Basic Res Cardiol 2003;98:210 -8.
- Dodoni G, Alexandre A, Di Lisa F. Formation of reactive oxygen species (ROS), mitochondrial dysfunction and cell death in H9c2 cardiomyoblasts. Biochim Biophys Acta 2004;1658:220 [Abstract].
- Zaccagnini G, Martelli F, Fasanaro P, Magenta A, Gaetano C, Di Carlo A, et al. p66ShcA modulates tissue response to hindlimb ischemia. Circulation 2004;109:2917 -23.
- Authors
- DILISA, F., & BERNARDI, P.
- Affiliations
- University of Padua (IT)
- ORCID
- BERNARDI, P
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2005-05-01
- Volume
- 66
- Issue
- 2
- Pages
- 222-232
- ISSN
- 0008-6363 (ISSN-L)
- OpenAlex
- W2130182990
- Cited by
- 139
- References
- 147
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 4 · 2022: 2 · 2021: 5 · 2020: 4 · 2019: 6 · 2018: 4 · 2017: 4 · 2016: 6 · 2015: 1 · 2014: 8 · 2013: 5 · 2012: 15
- FWCI
- 1.05
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cardiovascular Research (publishedVersion)
- PubMed (publishedVersion)
- Padua Research Archive (University of Padova) (submittedVersion, other-oa)
- INFM-OAR (INFN Catania) (submittedVersion, other-oa)
- Zenodo (CERN European Organization for Nuclear Research) (other-oa)
- Funders
- Ministero dell’Istruzione, dell’Università e della Ricerca
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial permeability transition pore, cardiac aging, mitochondrial dysfunction, respiratory chain deficiency, reactive oxygen species, mitochondrial DNA damage, ATP synthase, ischemic injury, aged heart
- MeSH terms
- Mitochondrial Permeability Transition Pore, Mitochondrial ADP, ATP Translocases, Aging, Calcium, DNA Damage, DNA, Mitochondrial, Electron Transport, Humans, Ion Channels, Mitochondria, Heart, Cell Death, Myocardial Ischemia, Reactive Oxygen Species, Oxidative Stress, Cell Respiration, Mitochondrial Membrane Transport Proteins
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