ReviewThe Journal of general physiology2025
How does mitochondrial Ca2+ change during ischemia and reperfusion? Implications for activation of the permeability transition pore.
Review in The Journal of general physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Mitochondrial oxidative stress, calcium and dynamics in cardiac ischaemia-reperfusion injury.The Journal of physiology · 2026Review
- Olaparib alleviates diclofenac-induced toxicity in HepG2 cells via modulation of oxidative stress and mitochondrial functions.Molecular and cellular biochemistry · 2026Article
- Synaptic mitochondria in aging and neurodegenerative diseases: Functional decline and vulnerability.Neural regeneration research · 2026Article
- Mitochondrial dysfunction in neonatal brain injury: from molecular mechanisms to therapeutic interventions.Journal of translational medicine · 2026Review
- Mechanisms of mitochondrial dysfunction and protective strategies in skin flap ischemia-reperfusion injury.Frontiers in pharmacology · 2026Review
- Mitochondrial Permeability Transition Pore: The Cardiovascular Disease's Molecular Achilles Heel.Biomedicines · 2025Review
- Mechano-energetic uncoupling in heart failure.Nature reviews. Cardiology · 2025Review
- Involvement of Oxidative Stress in Mitochondrial Abnormalities During the Development of Heart Disease.Biomedicines · 2025Review
- Calcium signaling in postsynaptic mitochondria: mechanisms, dynamics, and role in ATP production.Frontiers in molecular neuroscience · 2025Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Cardiac ischemia followed by reperfusion results in cardiac cell death, which has been attributed to an increase of mitochondrial Ca2+ concentration, resulting in activation of the mitochondrial permeability transition pore (PTP). Evaluating this hypothesis requires understanding of the mechanisms responsible for control of mitochondrial Ca2+ in physiological conditions and how they are altered during both ischemia and reperfusion. Ca2+ influx is thought to occur through the mitochondrial Ca2+ uniporter (MCU). However, with deletion of the MCU, an increase in mitochondrial Ca2+ still occurs, suggesting an alternative Ca2+ influx mechanism during ischemia. There is less certainty about the mechanisms responsible for Ca2+ efflux, with contributions from both Ca2+/H+ exchange and a Na+-dependent Ca2+ efflux pathway. The molecular details of both mechanisms are not fully resolved. We discuss this and the contributions of both pathways to the accumulation of mitochondrial Ca2+ during ischemia and reperfusion. We further discuss the role of mitochondrial Ca2+ in activation of the PTP.
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Registered trials
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