ReviewThe Biochemical journal2005
Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusion.
Review in The Biochemical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
93 citing papers in PubMed, 249 citations in OpenAlex.
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- Lipidomics of Caco-2 Cells Under Simulated Microgravity Conditions.International journal of molecular sciences · 2024Article
- A versatile delivery vehicle for cellular oxygen and fuels or metabolic sensor? A review and perspective on the functions of myoglobin.Physiological reviews · 2024Review
- Integrated transcriptome and metabolome analysis reveals the molecular responses of Pardosa pseudoannulata to hypoxic environments.BMC zoology · 2024Article
- Kazinol B protects H9c2 cardiomyocytes from hypoxia/reoxygenation-induced cardiac injury by modulating the AKT/AMPK/Nrf2 signalling pathway.Pharmaceutical biology · 2023Article
- The mitochondrial inhibitor IF1 binds to the ATP synthase OSCP subunit and protects cancer cells from apoptosis.Cell death & disease · 2023Article
- Mitochondrial ATP Synthase Tetramer Disassembly following Blood-Based or del Nido Cardioplegia during Neonatal Cardiac Surgery.The journal of extra-corporeal technology · 2022Article
- Mitochondrial CaInternational journal of molecular sciences · 2022Review
- The F1Fo-ATPase inhibitor protein IF1 in pathophysiology.Frontiers in physiology · 2022Review
- The Antioxidant Transcription Factor Nrf2 in Cardiac Ischemia-Reperfusion Injury.International journal of molecular sciences · 2021Review
- Mitochondria Isolated from Hearts Subjected to Ischemia/Reperfusion Benefit from Adenine Nucleotide Translocase 1 Overexpression.Membranes · 2021Article
- Review
- The ATP Synthase Deficiency in Human Diseases.Life (Basel, Switzerland) · 2021Review
- Analysis of human mitochondrial genome co-occurrence networks of Asian population at varying altitudes.Scientific reports · 2021Article
- New Insights Into the Role of Mitochondria Quality Control in Ischemic Heart Disease.Frontiers in cardiovascular medicine · 2021Review
- Augmented Cardiac Mitochondrial Capacity in High Capacity Aerobic Running "Disease-Resistant" Phenotype at Rest Is Lost Following Ischemia Reperfusion.Frontiers in cardiovascular medicine · 2021Article
- Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart tissue is remarkably sensitive to oxygen deprivation. Although heart cells, like those of most tissues, rapidly adapt to anoxic conditions, relatively short periods of ischaemia and subsequent reperfusion lead to extensive tissue death during cardiac infarction. Heart tissue is not readily regenerated, and permanent heart damage is the result. Although mitochondria maintain normal heart function by providing virtually all of the heart's ATP, they are also implicated in the development of ischaemic damage. While mitochondria do provide some mechanisms that protect against ischaemic damage (such as an endogenous inhibitor of the F1Fo-ATPase and antioxidant enzymes), they also possess a range of elements that exacerbate it, including ROS (reactive oxygen species) generators, the mitochondrial permeability transition pore, and their ability to release apoptotic factors. This review considers the process of ischaemic damage from a mitochondrial viewpoint. It considers ischaemic changes in the inner membrane complexes I-V, and how this might affect formation of ROS and high-energy phosphate production/degradation. We discuss the contribution of various mitochondrial cation channels to ionic imbalances which seem to be a major cause of reperfusion injury. The different roles of the H+, Ca2+ and the various K+ channel transporters are considered, particularly the K+(ATP) (ATP-dependent K+) channels. A possible role for the mitochondrial permeability transition pore in ischaemic damage is assessed. Finally, we summarize the metabolic and pharmacological interventions that have been used to alleviate the effects of ischaemic injury, highlighting the value of these or related interventions in possible therapeutics.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.