ArticleBasic research in cardiology2022
Extracellular stiffness induces contractile dysfunction in adult cardiomyocytes via cell-autonomous and microtubule-dependent mechanisms.
Article in Basic research in cardiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- T-tubular remodeling occurs in a cardiomyocyte-autonomous manner following pathological mechanical stiffness exposure.Journal of molecular and cellular cardiology plus · 2026Article
- Review
- Microtubule dynamics and post-translational modifications in cardiovascular diseases: mechanisms and therapeutic implications.Frontiers in cardiovascular medicine · 2026Review
- Direction-dependent contributions of cardiac myofilament networks to myocardial passive stiffness reveal a major disparity for titin.Basic research in cardiology · 2025Article
- Protein O-GlcNAcylation and hexokinase mitochondrial dissociation drive heart failure with preserved ejection fraction.Cell metabolism · 2025Article
- Article
- Article
- Vasohibin inhibition improves myocardial relaxation in a rat model of heart failure with preserved ejection fraction.Science translational medicine · 2024Article
- Focal Adhesion's Role in Cardiomyocytes Function: From Cardiomyogenesis to Mechanotransduction.Cells · 2024Review
- Distinct cytoskeletal regulators of mechanical memory in cardiac fibroblasts and cardiomyocytes.Basic research in cardiology · 2024Article
- Dynamic control of contractile resistance to iPSC-derived micro-heart muscle arrays.Journal of biomedical materials research. Part A · 2024Article
- Functional Impact of Alternative Metabolic Substrates in Failing Human Cardiomyocytes.JACC. Basic to translational science · 2024Article
- Adult human cardiomyocyte mechanics in osteogenesis imperfecta.American journal of physiology. Heart and circulatory physiology · 2023Article
- Biomechanical Impact of Pathogenic MYBPC3 Truncation Variant Revealed by Dynamically Tuning In Vitro Afterload.Journal of cardiovascular translational research · 2023Article
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8 authors.
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Abstract
The mechanical environment of the myocardium has a potent effect on cardiomyocyte form and function, yet an understanding of the cardiomyocyte responses to extracellular stiffening remains incomplete. We therefore employed a cell culture substrate with tunable stiffness to define the cardiomyocyte responses to clinically relevant stiffness increments in the absence of cell-cell interactions. When cultured on substrates magnetically actuated to mimic the stiffness of diseased myocardium, isolated rat adult cardiomyocytes exhibited a time-dependent reduction of sarcomere shortening, characterized by slowed contraction and relaxation velocity, and alterations of the calcium transient. Cardiomyocytes cultured on stiff substrates developed increases in viscoelasticity and microtubule detyrosination in association with early increases in the α-tubulin detyrosinating enzyme vasohibin-2 (Vash2). We found that knockdown of Vash2 was sufficient to preserve contractile performance as well as calcium transient properties in the presence of extracellular substrate stiffening. Orthogonal prevention of detyrosination by overexpression of tubulin tyrosine ligase (TTL) was also able to preserve contractility and calcium homeostasis. These data demonstrate that a pathologic increment of extracellular stiffness induces early, cell-autonomous remodeling of adult cardiomyocytes that is dependent on detyrosination of α-tubulin.
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