ReviewFrontiers in cardiovascular medicine2016
Mitochondrial Cardiomyopathies.
Review in Frontiers in cardiovascular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
107 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.
- Tumor Extracellular Vesicles Aggravate Mitochondrial Damage in Myocardial Ischemia/Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Pooled it
- Integration of multiple perspectives to understand the left ventricular pressure-volume relationship.Communications medicine · 2026Review
- Rethinking Left Ventricular Noncompaction and Excessive Left Ventricular Trabeculation: Development, Genetics, and a Proposed Conceptual Framework.Journal of clinical medicine · 2026Review
- Organelle network dysfunction in primary cardiomyopathy: An integrated perspective on pathogenesis and therapeutics.Journal of molecular and cellular cardiology plus · 2026Review
- TOP3A pathogenic variants presenting as dilated cardiomyopathy and heart failure in three pediatric cases.BMC pediatrics · 2026Article
- A large-scale multi-ancestry mitochondrial variant association analysis for cardiometabolic traits.Nature communications · 2026Article
- Mitochondrial cardiomyopathy: bridging molecular mechanisms and clinical frontiers.Nature reviews. Cardiology · 2026Review
- Hypoxia-driven microRNA-27b underlies pathologic cardiac endoreplication in heart disease.Signal transduction and targeted therapy · 2026Article
- Prenatal glucocorticoid exposure programs long-term left ventricular metabolism, function, and remodeling in baboons.American journal of physiology. Heart and circulatory physiology · 2026Article
- WASHC3 knockout disrupts mitochondrial protein homeostasis and energy metabolism in cardiomyocytes.Frontiers in cardiovascular medicine · 2026Article
- Hypertrophic Cardiomyopathy Phenocopies: Classification, Key Features, and Differential Diagnosis.Biomedicines · 2025Review
- Mitochondrial Dysfunction in Cardiomyopathy and Heart Failure: From Energetic Collapse to Therapeutic Opportunity.Biomolecules · 2025Review
- Cardiac magnetic resonance findings in mitochondrial disease: a guide for clinicians.European heart journal. Imaging methods and practice · 2025Review
- Genetic insights into hypertrophic cardiomyopathy: pathogenesis, diagnosis, and therapeutic implications.Journal of cardiovascular imaging · 2025Review
- Mitochondrial Dysfunction in Cardiac Surgery.Anesthesiology clinics · 2025Review
- A New Perspective on the Role of Alterations in Mitochondrial Proteins Involved in ATP Synthesis and Mobilization in Cardiomyopathies.International journal of molecular sciences · 2025Review
- Altered Fibroblast Glutamine Metabolism Is Linked to the Severity of Cardiac Dysfunction in DCMA, a Mitochondrial Cardiomyopathy.Journal of inherited metabolic disease · 2025Article
- Mitochondrial cardiomyopathies: navigating through different clinical and management pictures between adult and paediatric forms.Frontiers in cardiovascular medicine · 2025Review
- Severe bongkrekic acid poisoning caused by eating spoiled Auricularia auricula: a case report.BMC complementary medicine and therapies · 2024Article
- Article
47 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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are found in all nucleated human cells and perform various essential functions, including the generation of cellular energy. Mitochondria are under dual genome control. Only a small fraction of their proteins are encoded by mitochondrial DNA (mtDNA), whereas more than 99% of them are encoded by nuclear DNA (nDNA). Mutations in mtDNA or mitochondria-related nDNA genes result in mitochondrial dysfunction leading to insufficient energy production required to meet the needs for various organs, particularly those with high energy requirements, including the central nervous system, skeletal and cardiac muscles, kidneys, liver, and endocrine system. Because cardiac muscles are one of the high energy demanding tissues, cardiac involvement occurs in mitochondrial diseases with cardiomyopathies being one of the most frequent cardiac manifestations found in these disorders. Cardiomyopathy is estimated to occur in 20-40% of children with mitochondrial diseases. Mitochondrial cardiomyopathies can vary in severity from asymptomatic status to severe manifestations including heart failure, arrhythmias, and sudden cardiac death. Hypertrophic cardiomyopathy is the most common type; however, mitochondrial cardiomyopathies might also present as dilated, restrictive, left ventricular non-compaction, and histiocytoid cardiomyopathies. Cardiomyopathies are frequent manifestations of mitochondrial diseases associated with defects in electron transport chain complexes subunits and their assembly factors, mitochondrial transfer RNAs, ribosomal RNAs, ribosomal proteins, translation factors, mtDNA maintenance, and coenzyme Q10 synthesis. Other mitochondrial diseases with cardiomyopathies include Barth syndrome, Sengers syndrome, TMEM70-related mitochondrial complex V deficiency, and Friedreich ataxia.
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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.