ReviewFuture cardiology2012
Mitochondrial membrane permeabilization and cell death during myocardial infarction: roles of calcium and reactive oxygen species.
Review in Future cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 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
133 citing papers in PubMed, 293 citations in OpenAlex.
- TFEB Deficiency Impairs Male Fertility Through Mitochondrial Dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Phenolic-Rich Extracts from Artichoke By-Products Promote Apoptosis in Human Colorectal Cancer Cell Lines.Nutrients · 2026Article
- Research advances in intelligent microenvironment-responsive hydrogels for myocardial infarction therapy.APL bioengineering · 2026Review
- Exercise Improves Mitochondrial Homeostasis: A Potential Neuroprotective Strategy for Ischemic Stroke.Antioxidants (Basel, Switzerland) · 2026Review
- MG53, a Regenerative Myokine Linking Skeletal Muscle to Cardiac Repair.Biomolecules · 2026Review
- Myocardial Inflammation as Key Mediator of Heart-brain Interaction After Myocardial Ischemia/Infarction: Mechanistic Exploration of Post-Myocardial Infarction Cognitive Dysfunction.Current neuropharmacology · 2026Review
- NF-Frontiers in cardiovascular medicine · 2026Review
- Monitoring early micro-oxidation under refrigeration: iron and oxidative markers predict quality loss in grass carp.Current research in food science · 2026Article
- BAK and BAX: Therapeutic Targets for Acute Myocardial Infarction and Myocardial Ischemia-Reperfusion Injury.Biology · 2025Review
- In vivo imaging of reactive oxygen species after myocardial ischemia-reperfusion injury: a large animal multimodal imaging and transcriptomic study.bioRxiv : the preprint server for biology · 2025Article
- Effect of Functional Electrical Stimulation Combined With Physical Exercise on Electron Transport Chain Activity in Peripheral Blood Cells of Stroke Patients.Artificial organs · 2025Article
- Robinin attenuates cardiac oxidative stress-induced endoplasmic reticulum-dependent apoptosis through AKT/GSK3β pathway.Scientific reports · 2025Article
- Platelet Extracellular Vesicles as Natural Delivery Vehicles for Mitochondrial Dysfunction Therapy?ACS biomaterials science & engineering · 2025Review
- Aerosolized nicotine-free e-liquid base constituents exacerbates mitochondrial dysfunction and endothelial glycocalyx shedding via the AKT/GSK3β-mPTP pathway in lung injury models.Respiratory research · 2025Article
- Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions.Antioxidants (Basel, Switzerland) · 2025Review
- Calcium arrhythmogenicity of Purkinje fibers: importance of the animal model.Frontiers in physiology · 2025Review
- Exploring two tumor treatment strategies: effectiveness of ribosome inactivating proteins and mesenchymal stem cells/MSC derived extracellular vesicles in cancer treatment.Frontiers in oncology · 2025Review
- Cardioprotective effect of Robinin ameliorates Endoplasmic Reticulum Stress and Apoptosis in H9c2 cells.Cell biochemistry and biophysics · 2024Article
- Elucidation of the Active Agents in a West African Ground Herbal Medicine Formulation That Elicit Antimalarial Activities in In Vitro and In Vivo Models.Molecules (Basel, Switzerland) · 2024Article
- Mitochondrial Dysfunction in Systemic Lupus Erythematosus: Insights and Therapeutic Potential.Diseases (Basel, Switzerland) · 2024Review
73 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Excess generation of reactive oxygen species (ROS) and cytosolic calcium accumulation play major roles in the initiation of programmed cell death during acute myocardial infarction. Cell death may include necrosis, apoptosis and autophagy, and combinations thereof. During ischemia, calcium handling between the sarcoplasmic reticulum and myofilament is disrupted and calcium is diverted to the mitochondria causing swelling. Reperfusion, while essential for survival, reactivates energy transduction and contractility and causes the release of ROS and additional ionic imbalance. During acute ischemia-reperfusion, the principal death pathways are programmed necrosis and apoptosis through the intrinsic pathway, initiated by the opening of the mitochondrial permeability transition pore and outer mitochondrial membrane permeabilization, respectively. Despite intense investigation, the mechanisms of action and modes of regulation of mitochondrial membrane permeabilization are incompletely understood. Extrinsic apoptosis, necroptosis and autophagy may also contribute to ischemia-reperfusion injury. In this review, the roles of dysregulated calcium and ROS and the contributions of Bcl-2 proteins, as well as mitochondrial morphology in promoting mitochondrial membrane permeability change and the ensuing cell death during myocardial infarction are discussed.
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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.