ReviewCurrent opinion in genetics & development2016
Mitochondrial fission/fusion and cardiomyopathy.
Review in Current opinion in genetics & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- Mitochondrial quality control as a therapeutic target in cardiovascular disease: Mechanistic insights and future directions.Journal of translational internal medicine · 2025Article
- Comprehensive bioinformatics analysis and experimental verification identify mitochondrial gene Dgat2 as a novel therapeutic biomarker for myocardial ischemia-reperfusion.Frontiers in endocrinology · 2025Article
- Targeting mitochondrial transfer: a new horizon in cardiovascular disease treatment.Journal of translational medicine · 2024Review
- Late-life protein or isoleucine restriction impacts physiological and molecular signatures of aging.Nature aging · 2024Article
- Effect and mechanisms of Gambi-jung against high-fat diet-induced cardiac apoptosis in mice.Heliyon · 2024Article
- Late-life isoleucine restriction promotes physiological and molecular signatures of healthy aging.bioRxiv : the preprint server for biology · 2024Article
- Giant mitochondria in cardiomyocytes: cellular architecture in health and disease.Basic research in cardiology · 2023Review
- MALAT1/miR-185-5p mediated high glucose-induced oxidative stress, mitochondrial injury and cardiomyocyte apoptosis via the RhoA/ROCK pathway.Journal of cellular and molecular medicine · 2023Article
- Article
- Mitochondria Dysfunction at the Heart of Viral Myocarditis: Mechanistic Insights and Therapeutic Implications.Viruses · 2023Review
- Drp1 regulates transcription of ribosomal protein genes in embryonic hearts.Journal of cell science · 2022Article
- Long-Chain and Very Long-Chain Ceramides Mediate Doxorubicin-Induced Toxicity and Fibrosis.International journal of molecular sciences · 2021Article
- A Novel Role of Claudin-5 in Prevention of Mitochondrial Fission Against Ischemic/Hypoxic Stress in Cardiomyocytes.The Canadian journal of cardiology · 2021Article
- Age-related decline in murine heart and skeletal muscle performance is attenuated by reduced Ahnak1 expression.Journal of cachexia, sarcopenia and muscle · 2021Article
- Therapeutic potential and recent advances on targeting mitochondrial dynamics in cardiac hypertrophy: A concise review.Molecular therapy. Nucleic acids · 2021Review
- Cardiolipin Remodeling Defects Impair Mitochondrial Architecture and Function in a Murine Model of Barth Syndrome Cardiomyopathy.Circulation. Heart failure · 2021Article
- Molecular Epidemiology of Mitochondrial Cardiomyopathy: A Search Among Mitochondrial and Nuclear Genes.International journal of molecular sciences · 2021Review
- Myofibril and mitochondria morphogenesis are coordinated by a mechanical feedback mechanism in muscle.Nature communications · 2021Article
- Cardiac GRK2 Protein Levels Show Sexual Dimorphism during Aging and Are Regulated by Ovarian Hormones.Cells · 2021Article
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
Abstract
Mitochondria are highly abundant in and essential to the beat-to-beat contractile performance of hearts. However, relatively few cardiac diseases have been attributed to primary mitochondrial dysfunction. The paucity of evidence for 'primary mitochondrial cardiac diseases' may be because such an entity does not exist. Alternately, the consequences of mitochondrial dysfunction on hearts may be so severe that long-term viability is severely impaired and affected individuals are therefore not included in standard genetic screens of adult heart disease subjects. Here, I review accumulating experimental evidence that impairing mitochondrial fission or fusion causes cardiomyopathy in otherwise normal mice, and consider how these data could motivate screening of perinatal cardiomyopathy subjects for damaging mutations of mitochondrial fission and fusion factors.
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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.