ArticleExperimental physiology2019
Cardiac-specific overexpression of caveolin-3 preserves t-tubular I
Article in Experimental physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- The β1 adrenoceptor (AR) blocker metoprolol normalises βAR cascade and caveolar protein expression and restores β1AR responsiveness in failing right ventricular myocytes.Journal of molecular and cellular cardiology plus · 2026Article
- Assessment of serum caveolin-3 levels in patients with heart failure.Frontiers in cardiovascular medicine · 2025Article
- Membrane remodelling triggers maturation of excitation-contraction coupling in 3D-shaped human-induced pluripotent stem cell-derived cardiomyocytes.Basic research in cardiology · 2023Article
- Evolution of the cardiac dyad.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Heat Shock Protein 90 as Therapeutic Target for CVDs and Heart Ageing.International journal of molecular sciences · 2022Review
- The Physiology and Pathophysiology of T-Tubules in the Heart.Frontiers in physiology · 2021Review
- Glucocorticoids preserve the t-tubular system in ventricular cardiomyocytes by upregulation of autophagic flux.Basic research in cardiology · 2019Article
- Cardiac-specific overexpression of caveolin-3 preserves t-tubular IExperimental physiology · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
NEW
findingsWhat is the central question of this study? What is the cellular basis of the protection conferred on the heart by overexpression of caveolin-3 (Cav-3 OE) against many of the features of heart failure normally observed in vivo? What is the main finding and its importance? Cav-3 overexpression has little effect in normal ventricular myocytes but reduces cellular hypertrophy and preserves t-tubular I ABSTRACT: Caveolin-3 (Cav-3) is an 18 kDa protein that has been implicated in t-tubule formation and function in cardiac ventricular myocytes. During cardiac hypertrophy and failure, Cav-3 expression decreases, t-tubule structure is disrupted and excitation-contraction coupling (ECC) is impaired. Previous work has suggested that Cav-3 overexpression (OE) is cardio-protective, but the effect of Cav-3 OE on these cellular changes is unknown. We therefore investigated whether Cav-3 OE in mice is protective against the cellular effects of pressure overload induced by 8 weeks' transverse aortic constriction (TAC). Cav-3 OE mice developed cardiac dilatation, decreased stroke volume and ejection fraction, and hypertrophy and pulmonary congestion in response to TAC. These changes were accompanied by cellular hypertrophy, a decrease in t-tubule regularity and density, and impaired local Ca
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