ReviewBiochimica et biophysica acta2011
What makes the mitochondria a killer? Can we condition them to be less destructive?
Review in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed.
- Medicinal Plants and Phytochemicals in Cardioprotection-Mechanistic Pathways and Translational Roadmap.Life (Basel, Switzerland) · 2026Review
- Key Mechanisms of Oxidative Stress-Induced Ferroptosis in Heart Failure with Preserved Ejection Fraction and Potential Therapeutic Approaches.Reviews in cardiovascular medicine · 2025Review
- Monitoring mitochondrial calcium in cardiomyocytes during coverslip hypoxia using a fluorescent lifetime indicator.Journal of molecular and cellular cardiology plus · 2024Article
- Organ-Specific Mitochondrial Alterations Following Ischemia-Reperfusion Injury in Post-Cardiac Arrest Syndrome: A Comprehensive Review.Life (Basel, Switzerland) · 2024Review
- Increased mitochondrial free CaCell reports · 2023Article
- Review
- Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning.International journal of molecular sciences · 2022Review
- Therapeutic Peptides to Treat Myocardial Ischemia-Reperfusion Injury.Frontiers in cardiovascular medicine · 2022Review
- Editorial: Role of mitochondria-associated non-coding RNAs in intracellular communication.Frontiers in physiology · 2022Article
- Regulation of Mitochondrial CaAnnual review of physiology · 2021Review
- Nuclear-mitochondrial communication involving miR-181c plays an important role in cardiac dysfunction during obesity.Journal of molecular and cellular cardiology · 2020Article
- Role of Mitochondrial Calcium and the Permeability Transition Pore in Regulating Cell Death.Circulation research · 2020Review
- Ischemia Reperfusion Injury: Mechanisms of Damage/Protection and Novel Strategies for Cardiac Recovery/Regeneration.International journal of molecular sciences · 2019Review
- Fmr1 protects cardiomyocytes against lipopolysaccharide-induced myocardial injury.Experimental and therapeutic medicine · 2018Article
- Does p53 Inhibition Suppress Myocardial Ischemia-Reperfusion Injury?Journal of cardiovascular pharmacology and therapeutics · 2018Article
- Mitochondria in Cardiac Postconditioning.Frontiers in physiology · 2018Review
- Using chemical biology to assess and modulate mitochondria: progress and challenges.Interface focus · 2017Review
- Mitochondrial Dysfunction and Myocardial Ischemia-Reperfusion: Implications for Novel Therapies.Annual review of pharmacology and toxicology · 2017Review
- Mitochondrial Bioenergetics Is Altered in Fibroblasts from Patients with Sporadic Alzheimer's Disease.Frontiers in neuroscience · 2017Article
- Ischemia/Reperfusion Injury following Acute Myocardial Infarction: A Critical Issue for Clinicians and Forensic Pathologists.Mediators of inflammation · 2017 · on this mapReview
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.
Funding
Abstract
Cardioprotection, such as preconditioning and postconditioning, has been shown to result in a significant reduction in cell death. Many of the signaling pathways activated by cardioprotection have been elucidated, but there is still a lack of understanding of the mechanisms by which these signaling pathways reduce cell death. Mitochondria have been reported to be an important player in many types of apoptotic and necrotic cell death. If mitochondria play an important role in cell death, then it seems reasonable to consider that cardioprotective mechanisms might act, at least in part, by opposing mitochondrial cell death pathways. One of the major mechanisms of cell death in ischemia-reperfusion is suggested to be the opening of a large conductance pore in the inner mitochondrial membrane, known as the mitochondrial permeability transition pore. Inhibition of this mitochondrial pore appears to be one of the major mechanisms by which cardioprotection reduces cell death. Cardioprotection activates a number of signaling pathways that reduce the level of triggers (reactive oxygen species and calcium) or enhances inhibitors of the mitochondrial permeability transition pore at the start of reperfusion. This article is part of a Special Issue entitled: Mitochondria and Cardioprotection.
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What OpenQuestion holds
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.