ReviewReviews in cardiovascular medicine2023
Mitochondrial Dysfunction in Arrhythmia and Cardiac Hypertrophy.
Review in Reviews in cardiovascular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed.
- Association Between Endogenous Ketosis and Risk of Atrial Fibrillation in Intensive Care Versus General Ward Patients: A Retrospective Cohort Study.Journal of clinical medicine · 2026Article
- Beyond energy production: targeting mitochondrial biogenesis in aging and cancer with phytochemical intervention.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Electrophysiological and Molecular Features of Remdesivir-Induced Cardiac Toxicity in Male and Female Guinea Pigs.International journal of molecular sciences · 2026Article
- PKA activation rescues myocardial injury elicited by silica nanoparticles through improving oxidative stress, mitochondrial health, and copper homeostasis.Materials today. Bio · 2026Article
- Ion channels and cardiac disease: mechanisms and functions of a disintegrin and metalloproteases and their substrates.Frontiers in cell and developmental biology · 2026Review
- ID2 attenuates post-MI ventricular arrhythmias by targeting GATA4 suppression to preserve mitochondrial function and NaOpen medicine (Warsaw, Poland) · 2026Article
- Acute and prolonged effects of anti-malarial drugs on mitochondrial respiration in atrial cardiomyocytes for cardiac safety evaluation.PloS one · 2026Article
- Mesencephalic Astrocyte-Derived Neurotrophic Factor Binds BAX to Preserve Mitochondrial Homeostasis and Energy Metabolism for Relieving Myocardial Hypertrophy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mitochondrial DNA Dysfunction in Cardiovascular Diseases: A Novel Therapeutic Target.Antioxidants (Basel, Switzerland) · 2025Review
- Elevated levels of Letm1 drives mitochondrial dysfunction and cardiomyocyte stress-mediated apoptosis in cultured cardiomyocytes.Cell communication and signaling : CCS · 2025Article
- Homocysteine promotes cardiomyocyte hypertrophy through inhibiting β-catenin/ FUNDC1 mediated mitophagy.Scientific reports · 2025Article
- Mitochondrial Dysfunction in Endothelial Cells: A Key Driver of Organ Disorders and Aging.Antioxidants (Basel, Switzerland) · 2025Review
- Dilated Cardiomyopathy May Be Associated With a Novel Mitochondrial tRNAHuman mutation · 2025Article
- Redox Homeostasis and Molecular Biomarkers in Precision Therapy for Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arrhythmia and cardiac hypertrophy are two very common cardiovascular diseases that can lead to heart failure and even sudden death, thus presenting a serious threat to human life and health. According to global statistics, nearly one million people per year die from arrhythmia, cardiac hypertrophy and other associated cardiovascular diseases. Hence, there is an urgent need to find new treatment targets and to develop new intervention measures. Recently, mitochondrial dysfunction has been examined in relation to heart disease with a view to lowering the incidence of arrhythmia and cardiac hypertrophy. The heart is the body's largest energy consuming organ, turning over about 20 kg of adenosine triphosphate (ATP) per day in the mitochondria. Mitochondrial oxidative phosphorylation (OXPHOS) produces up to 90% of the ATP needed by cardiac muscle cells for contraction and relaxation. Dysfunction of heart mitochondria can therefore induce arrhythmia, cardiac hypertrophy and other cardiovascular diseases. Mitochondrial
Indexed as
Identifiers
What Socratic 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 Socratic graph.