ReviewCardiovascular research2010
Cardiac mitochondria and arrhythmias.
Review in Cardiovascular research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 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
126 citing papers in PubMed, 220 citations in OpenAlex.
- CYP2D6 as an Emerging Endogenous Oxidative Stress Modulator in Cardiovascular Disease: Genetic, Pharmacological, and Redox Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- Obstructive Sleep Apnea and Arrhythmia: A Narrative Review of Arrhythmogenic Mechanisms.Diagnostics (Basel, Switzerland) · 2026Review
- Theoretical quantitative model and clinical outcome predictions of conductive cardiac patches for electrophysiological treatments.Nature biomedical engineering · 2026Article
- Resistance Exercise: A Potential Intervention for Managing Cardiovascular Health in Individuals with a History of Cancer.Sports medicine - open · 2026Article
- Redox Imbalance in the Cardiohepatic Syndrome: The Emerging Role of Oxidative Stress in Cirrhosis-Associated Cardiac Dysfunction.Antioxidants (Basel, Switzerland) · 2026Review
- Cardiac resident macrophages: the emerging role in arrhythmogenesis.Frontiers in immunology · 2026Review
- Increased Intermembrane Space [CaCirculation research · 2025Article
- Mitochondrial Dysfunction in Cardiomyopathy and Heart Failure: From Energetic Collapse to Therapeutic Opportunity.Biomolecules · 2025Review
- Mitochondrial Dysfunction in the Cardiovascular Disease Continuum: Problems of Studying the Progression During the Follow-Up of the Pathologies.International journal of molecular sciences · 2025Review
- Dapagliflozin alleviates mitochondrial damage in the myocardium under diabetic conditions by targeting sortilin.Cellular and molecular life sciences : CMLS · 2025Article
- Article
- Improving effect of physical exercise on heart failure: Reducing oxidative stress-induced inflammation by restoring CaMolecular and cellular biochemistry · 2025Review
- TAB2 deficiency induces dilated cardiomyopathy by promoting mitochondrial calcium overload in human iPSC-derived cardiomyocytes.Molecular medicine (Cambridge, Mass.) · 2025Article
- Mitochondrial complex-1 as a therapeutic target for cardiac diseases.Molecular and cellular biochemistry · 2025Review
- Mitochondrial diseases: from molecular mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Importance of Zinc Homeostasis for Normal Cardiac Rhythm.Current cardiology reviews · 2025Review
- Pathological Alterations in Heart Mitochondria in a Rat Model of Isoprenaline-Induced Myocardial Injury and Their Correction with Water-Soluble Taxifolin.International journal of molecular sciences · 2024Article
- Implications for neutrophils in cardiac arrhythmias.American journal of physiology. Heart and circulatory physiology · 2024Review
- Mitochondrial Dysfunction in Heart Failure: From Pathophysiological Mechanisms to Therapeutic Opportunities.International journal of molecular sciences · 2024Review
- Cardiac arrhythmogenesis: roles of ion channels and their functional modification.Frontiers in physiology · 2024Review
66 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 1 country.
Funding
Abstract
Despite a high prevalence of sudden cardiac death throughout the world, the mechanisms that lead to ventricular arrhythmias are not fully understood. Over the last 20 years, a growing body of evidence indicates that cardiac mitochondria are involved in the genesis of arrhythmia. In this review, we have attempted to describe the role that mitochondria play in altering the heart's electrical function by introducing heterogeneity into the cardiac action potential. Specifically, we have focused on how the energetic status of the mitochondrial network can alter sarcolemmal potassium fluxes through ATP-sensitive potassium channels, creating a 'metabolic sink' for depolarizing wave-fronts and introducing conditions that favour catastrophic arrhythmia. Mechanisms by which mitochondria depolarize under conditions of oxidative stress are characterized, and the contributions of several mitochondrial ion channels to mitochondrial depolarization are presented. The inner membrane anion channel in particular opens upstream of other inner membrane channels during metabolic stress, and may be an effective target to prevent the metabolic oscillations that create action potential lability. Finally, we discuss therapeutic strategies that prevent arrhythmias by preserving mitochondrial membrane potential in the face of oxidative stress, supporting the notion that treatments aimed at cardiac mitochondria have significant potential in attenuating electrical dysfunction in the heart.
Indexed as
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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.