ReviewJournal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing2013
Mitochondrial targets for arrhythmia suppression: is there a role for pharmacological intervention?
Review in Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 11 citations in OpenAlex.
- Mitochondrial network remodeling of the diabetic heart: implications to ischemia related cardiac dysfunction.Cardiovascular diabetology · 2024Review
- Mechanisms Underlying Antiarrhythmic Properties of Cardioprotective Agents Impacting Inflammation and Oxidative Stress.International journal of molecular sciences · 2022Review
- Pro-Arrhythmic Signaling of Thyroid Hormones and Its Relevance in Subclinical Hyperthyroidism.International journal of molecular sciences · 2020Review
- Late-onset multiple acyl-CoA dehydrogenase deficiency with cardiac syncope: A case report.World journal of clinical cases · 2020Article
- Proarrhythmic Remodeling of Calcium Homeostasis in Cardiac Disease; Implications for Diabetes and Obesity.Frontiers in physiology · 2018Review
- Omega-3 Index and Anti-Arrhythmic Potential of Omega-3 PUFAs.Nutrients · 2017Review
- SK channel enhancers attenuate Ca2+-dependent arrhythmia in hypertrophic hearts by regulating mito-ROS-dependent oxidation and activity of RyR.Cardiovascular research · 2017Article
- Functional Role of Mitochondria in Arrhythmogenesis.Advances in experimental medicine and biology · 2017Review
- The mitochondrial translocator protein and arrhythmogenesis in ischemic heart disease.Oxidative medicine and cellular longevity · 2015Review
- Functional crosstalk between the mitochondrial PTP and KATP channels determine arrhythmic vulnerability to oxidative stress.Frontiers in physiology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction is a hallmark of common cardiovascular disorders, including ischemia-reperfusion injury, hypertrophy, heart failure, and diabetes mellitus. While the role of the mitochondrial network in regulating energy production and cell death pathways is well established, its active control of other critical cellular functions, including excitation-contraction coupling and excitability, is less understood. The purpose of this focused review article is to highlight the growing mechanistic link between mitochondrial dysfunction and arrhythmogenesis. The goal is not to provide a comprehensive listing of all factors by which mitochondrial bioenergetics and altered cellular redox status affect ion channel function but rather to focus on one central mechanism of arrhythmogenesis which arises from a mitochondrial origin. In doing so, we discuss the role of mitochondrial targets for suppressing arrhythmias through this mechanism.
Indexed as
Identifiers
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.