ReviewPharmacology & therapeutics2011
Mitochondria are sources of metabolic sink and arrhythmias.
Review in Pharmacology & therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 72 citations in OpenAlex.
- Physical frailty, genetic predisposition, and incident arrhythmias.Journal of cachexia, sarcopenia and muscle · 2024Article
- Mitochondrial network remodeling of the diabetic heart: implications to ischemia related cardiac dysfunction.Cardiovascular diabetology · 2024Review
- Cardiac arrhythmogenesis: roles of ion channels and their functional modification.Frontiers in physiology · 2024Review
- mROS‑calcium feedback loop promotes lethal ventricular arrhythmias and sudden cardiac death in early myocardial ischemia.International journal of molecular medicine · 2024Article
- Serum albumin levels and risk of atrial fibrillation: a Mendelian randomization study.Frontiers in cardiovascular medicine · 2024Article
- Small-conductance calcium-activated potassium channels in the heart: expression, regulation and pathological implications.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Cardiomyocyte electrophysiology and its modulation: current views and future prospects.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Review
- Anti-malarial drugs: Mechanisms underlying their proarrhythmic effects.British journal of pharmacology · 2022Review
- Mechanisms Underlying Antiarrhythmic Properties of Cardioprotective Agents Impacting Inflammation and Oxidative Stress.International journal of molecular sciences · 2022Review
- Evidence for the Benefits of Melatonin in Cardiovascular Disease.Frontiers in cardiovascular medicine · 2022Review
- Mitochondrial Dysfunction Increases Arrhythmic Triggers and Substrates; Potential Anti-arrhythmic Pharmacological Targets.Frontiers in cardiovascular medicine · 2021Review
- Emerging Role of Mitophagy in the Heart: Therapeutic Potentials to Modulate Mitophagy in Cardiac Diseases.Oxidative medicine and cellular longevity · 2021Review
- Cardiac Connexin-43 Hemichannels and Pannexin1 Channels: Provocative Antiarrhythmic Targets.International journal of molecular sciences · 2020Review
- The debate continues - What is the role of MCU and mitochondrial calcium uptake in the heart?Journal of molecular and cellular cardiology · 2020Review
- Pro-Arrhythmic Signaling of Thyroid Hormones and Its Relevance in Subclinical Hyperthyroidism.International journal of molecular sciences · 2020Review
- Molecular basis of arrhythmic substrate in ageing murine peroxisome proliferator-activated receptor γ co-activator deficient hearts modelling mitochondrial dysfunction.Bioscience reports · 2019Article
- Association Between Antiarrhythmic, Electrophysiological, and Antioxidative Effects of Melatonin in Ischemia/Reperfusion.International journal of molecular sciences · 2019Article
- Atrial Transcriptional Profiles of Molecular Targets Mediating Electrophysiological Function in Aging andFrontiers in physiology · 2019Article
- Gene and Protein Expression Profile of Selected Molecular Targets Mediating Electrophysiological Function inInternational journal of molecular sciences · 2018Article
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 1 institution in 1 country.
Funding
Abstract
Mitochondria have long been recognized for their central role in energy transduction and apoptosis. More recently, extensive work in multiple laboratories around the world has significantly extended the role of cardiac mitochondria from relatively static arbitrators of cell death and survival pathways to highly dynamic organelles that form interactive functional networks across cardiomyocytes. These coupled networks were shown to strongly affect cardiomyocyte responses to oxidative stress by modulating cell signaling pathways that strongly impact physiological properties. Of particular importance is the role of mitochondria in modulating key electrophysiological and calcium cycling properties in cardiomyocytes, either directly through activation of a myriad of mitochondrial ion channels or indirectly by affecting cell signaling cascades, ATP levels, and the over-all redox state of the cardiomyocyte. This important recognition has ushered a renewed interest in understanding, at a more fundamental level, the exact role that cardiac metabolism, in general and mitochondria, in particular, play in both health and disease. In this article, we provide an overview of recent advances in our growing understanding of the fundamental role that cardiac mitochondria play in the genesis of lethal arrhythmias.
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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.