ReviewFrontiers in cardiovascular medicine2021
Mitochondria in Pathological Cardiac Hypertrophy Research and Therapy.
Review in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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
33 citing papers in PubMed, 59 citations in OpenAlex.
- YAP and WWTR1/TAZ Connect Mechanotransduction and Mitochondrial Metabolism in Cardiac Hypertrophy and Ventricular Remodeling.Journal of cardiovascular translational research · 2026Review
- Targeting mitochondrial morphofunctional homeostasis and oxidative stress: Iristectorigenin A protects against cardiac remodeling via SIRT6/FOXO1 signaling.Acta pharmacologica Sinica · 2026Article
- Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies.Cardiovascular drugs and therapy · 2026Review
- ABCC9 knockdown attenuates isoproterenol‑induced myocardial hypertrophy by inhibiting the PI3K/AKT signaling pathway.Molecular medicine reports · 2026Article
- Energy Metabolism Under Stress: Late-Stage Leigh Syndrome Reveals Profound Cardiometabolic Perturbations in Ndufs4 KO Mice.Journal of inherited metabolic disease · 2026Article
- PHB2 protects against pressure overload-induced myocardial remodeling in mice via stabilizing TOMM40 and regulating mitochondrial morphofunctional homeostasis.Acta pharmacologica Sinica · 2025Article
- 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
- The Role of Mitochondrial Dysfunction and Dynamics in Hypertensive Heart Disease: Mechanisms and Recent Advances.Biology · 2025Review
- Identification of novel MYO19 variants in neonatal hypertrophic cardiomyopathy: a familial analysis revealing oligogenic contributors to disease severity.Orphanet journal of rare diseases · 2025Article
- Colonization withbioRxiv : the preprint server for biology · 2025Article
- The potential value of microRNA-409-5p-mediated negative regulation of USP7 in the diagnosis and treatment of acute myocardial infarction.BMC cardiovascular disorders · 2025Article
- Diminazine protects against cardiac aging through the improvement of mitophagy and apoptosis in aging rats induced by D-galactose.BMC cardiovascular disorders · 2025Article
- Regulatory mechanisms of exercise-induced physiological cardiac hypertrophy: progress and prospects.Frontiers in cardiovascular medicine · 2025Review
- Article
- Opa1 processing is dispensable in mouse development but is protective in mitochondrial cardiomyopathy.Science advances · 2024Article
- Large animal models of pressure overload-induced cardiac left ventricular hypertrophy to study remodelling of the human heart with aortic stenosis.Cardiovascular research · 2024Review
- Mitochondrial dysfunction is associated with hypertrophic cardiomyopathy in Pompe disease-specific induced pluripotent stem cell-derived cardiomyocytes.Cell proliferation · 2024Article
- The role of deubiquitinases in cardiac disease.Expert reviews in molecular medicine · 2024Review
- Molecular and Cellular Mechanisms Underlying the Cardiac Hypertrophic and Pro-Remodelling Effects of Leptin.International journal of molecular sciences · 2024Review
- Editorial: Mitochondrial plasticity and quality control in health and disease.Frontiers in cell and developmental biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy, a stereotypic cardiac response to increased workload, ultimately progresses to severe contractile dysfunction and uncompensated heart failure without appropriate intervention. Sustained cardiac overload inevitably results in high energy consumption, thus breaking the balance between mitochondrial energy supply and cardiac energy demand. In recent years, accumulating evidence has indicated that mitochondrial dysfunction is implicated in pathological cardiac hypertrophy. The significant alterations in mitochondrial energetics and mitochondrial proteome composition, as well as the altered expression of transcripts that have an impact on mitochondrial structure and function, may contribute to the initiation and progression of cardiac hypertrophy. This article presents a summary review of the morphological and functional changes of mitochondria during the hypertrophic response, followed by an overview of the latest research progress on the significant modulatory roles of mitochondria in cardiac hypertrophy. Our article is also to summarize the strategies of mitochondria-targeting as therapeutic targets to treat cardiac hypertrophy.
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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.