ReviewJournal of molecular and cellular cardiology plus2023
Mechano-energetic uncoupling in hypertrophic cardiomyopathy: Pathophysiological mechanisms and therapeutic opportunities.
Review in Journal of molecular and cellular cardiology plus, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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Who cites it
12 citing papers in PubMed.
- Myofilament-level effects of aficamten increase diastolic chamber volumes and maintain cardiac output through preserved length-dependent force generation in healthy rat and canine myocardium.Basic research in cardiology · 2026Article
- Immature and mature myocardium in the pathophysiology of hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2026Review
- SGLT2 Inhibitors in Hypertrophic Cardiomyopathy: Emerging Evidence and Putative Mechanisms.Biomolecules · 2026Review
- Why the septum thickens in hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2026Review
- Changes in cardiac myosin acetylation disrupt the super-relaxed state in genotype-negative hypertrophic cardiomyopathy with type 2 diabetes.Cardiovascular diabetology · 2026Article
- Mitochondrial Dysfunction in Cardiomyopathy and Heart Failure: From Energetic Collapse to Therapeutic Opportunity.Biomolecules · 2025Review
- The Utility of Nuclear Imaging in Hypertrophic Cardiomyopathy: A Narrative Review.Journal of clinical medicine · 2025Review
- Hypertrophic Cardiomyopathy Through the Lens of Mitochondria.Biomedicines · 2025Review
- Hyperpolarized-MRI in Hypertrophic Cardiomyopathy: A Narrative Review.Clinical Medicine Insights. Cardiology · 2025Review
- Notch2 Signaling Drives Cardiac Hypertrophy by Suppressing Purine Nucleotide Metabolism.Research (Washington, D.C.) · 2025Article
- Definitional Challenges in Understanding Hypertrophic Cardiomyopathy.Diagnostics (Basel, Switzerland) · 2024Review
- Genetic Mutations and Mitochondrial Redox Signaling as Modulating Factors in Hypertrophic Cardiomyopathy: A Scoping Review.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertrophic cardiomyopathy (HCM) is a frequent inherited form of heart failure. The underlying cause of HCM is generally attributed to mutations in genes that encode for sarcomeric proteins, but the pathogenesis of the disease is also influenced by non-genetic factors, which can contribute to diastolic dysfunction and hypertrophic remodeling. Central to the pathogenesis of HCM is hypercontractility, a state that is an antecedent to several key derangements, including increased mitochondrial workload and oxidative stress. As a result, energy depletion and mechano-energetic uncoupling drive cardiac growth through signaling pathways such as ERK and/or potentially AMPK downregulation. Metabolic remodeling also occurs in HCM, characterized by decreased fatty acid oxidation and increased glucose uptake. In some instances, ketones may also feed the heart with energy and act as signaling molecules to reduce oxidative stress and hypertrophic signaling. In addition, arrhythmias are frequently triggered in HCM, resulting from the high Ca
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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.