ArticleJournal of molecular and cellular cardiology2014
Caveolae in ventricular myocytes are required for stretch-dependent conduction slowing.
Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 47 citations in OpenAlex.
- Caveolar Compartmentalization of Pacemaker Signaling Ensures Stable Sinoatrial Rhythmicity Which Is Disrupted in Heart Failure.JACC. Clinical electrophysiology · 2026Article
- New mesenchymal stem/stromal cell-based strategies for osteoarthritis treatment: targeting macrophage-mediated inflammation to restore joint homeostasis.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Stretch regulation of β2-Adrenoceptor signalling in cardiomyocytes requires caveolae.Cardiovascular research · 2025Article
- Mitochondrial Transplantation: A Paradigm Shift in Osteoporosis Therapy.International journal of nanomedicine · 2025Review
- Neutral sphingomyelinase regulates mechanotransduction in human engineered cardiac tissues and mouse hearts.The Journal of physiology · 2024Article
- Mechanisms of stretch-induced electro-anatomical remodeling and atrial arrhythmogenesis.Journal of molecular and cellular cardiology · 2024Review
- Differential sensitivity to longitudinal and transverse stretch mediates transcriptional responses in mouse neonatal ventricular myocytes.American journal of physiology. Heart and circulatory physiology · 2024Article
- Caveolae-associated cAMP/CaJournal of molecular and cellular cardiology · 2023Article
- Mitochondrial dysfunction in neurodegenerative disorders: Potential therapeutic application of mitochondrial transfer to central nervous system-residing cells.Journal of translational medicine · 2023Review
- Mitochondrial transplantation as a promising therapy for mitochondrial diseases.Acta pharmaceutica Sinica. B · 2023Review
- Active force generation contributes to the complexity of spontaneous activity and to the response to stretch of murine cardiomyocyte cultures.The Journal of physiology · 2022Article
- Caveolin-3 prevents swelling-induced membrane damage via regulation of IBiophysical journal · 2022Article
- Review
- Beat-by-Beat Cardiomyocyte T-Tubule Deformation Drives Tubular Content Exchange.Circulation research · 2021Article
- Computationally efficient model of myocardial electromechanics for multiscale simulations.PloS one · 2021Article
- Novel Optics-Based Approaches for Cardiac Electrophysiology: A Review.Frontiers in physiology · 2021Review
- Mitochondrial donation in translational medicine; from imagination to reality.Journal of translational medicine · 2020Review
- Sinoatrial Node Structure, Mechanics, Electrophysiology and the Chronotropic Response to Stretch in Rabbit and Mouse.Frontiers in physiology · 2020Article
- The Role of Membrane Capacitance in Cardiac Impulse Conduction: An Optogenetic Study With Non-excitable Cells Coupled to Cardiomyocytes.Frontiers in physiology · 2020Article
- Caveolae-Mediated Activation of Mechanosensitive Chloride Channels in Pulmonary Veins Triggers Atrial Arrhythmogenesis.Journal of the American Heart Association · 2019Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Mechanical stretch of cardiac muscle modulates action potential propagation velocity, causing potentially arrhythmogenic conduction slowing. The mechanisms by which stretch alters cardiac conduction remain unknown, but previous studies suggest that stretch can affect the conformation of caveolae in myocytes and other cell types. We tested the hypothesis that slowing of action potential conduction due to cardiac myocyte stretch is dependent on caveolae. Cardiac action potential propagation velocities, measured by optical mapping in isolated mouse hearts and in micropatterned mouse cardiomyocyte cultures, decreased reversibly with volume loading or stretch, respectively (by 19±5% and 26±4%). Stretch-dependent conduction slowing was not altered by stretch-activated channel blockade with gadolinium or by GsMTx-4 peptide, but was inhibited when caveolae were disrupted via genetic deletion of caveolin-3 (Cav3 KO) or membrane cholesterol depletion by methyl-β-cyclodextrin. In wild-type mouse hearts, stretch coincided with recruitment of caveolae to the sarcolemma, as observed by electron microscopy. In myocytes from wild-type but not Cav3 KO mice, stretch significantly increased cell membrane capacitance (by 98±64%), electrical time constant (by 285±149%), and lipid recruitment to the bilayer (by 84±39%). Recruitment of caveolae to the sarcolemma during physiologic cardiomyocyte stretch slows ventricular action potential propagation by increasing cell membrane capacitance.
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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.