ArticleJournal of the American College of Cardiology2011
Cardiac-specific overexpression of caveolin-3 attenuates cardiac hypertrophy and increases natriuretic peptide expression and signaling.
Article in Journal of the American College of Cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 93 citations in OpenAlex.
- 2-MCPD-Induced Effects in the Heart: Toxicological and Mechanistic Implications from Comparative Proteomic Analyses in Rats.Molecules (Basel, Switzerland) · 2026Article
- Role of membrane microdomains in cardiac protection: strategies for diabetic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2025Review
- Microbiota-indole-3-propionic acid-heart axis mediates the protection of leflunomide against αPD1-induced cardiotoxicity in mice.Nature communications · 2025Article
- Assessment of serum caveolin-3 levels in patients with heart failure.Frontiers in cardiovascular medicine · 2025Article
- Identification of Prominin-2 as a new player of cardiomyocyte senescence in the aging heart.Aging cell · 2024Article
- Mechanisms of stretch-induced electro-anatomical remodeling and atrial arrhythmogenesis.Journal of molecular and cellular cardiology · 2024Review
- Fibroblast-localized lncRNA CFIRL promotes cardiac fibrosis and dysfunction in dilated cardiomyopathy.Science China. Life sciences · 2024Article
- ROCK1 deficiency preserves caveolar compartmentalization of signaling molecules and cell membrane integrity.FASEB bioAdvances · 2024Article
- Caveolin-3 and Caveolae regulate ventricular repolarization.Journal of molecular and cellular cardiology · 2023Article
- Changes in cellular CaThe Journal of physiology · 2023Article
- Article
- The importance of caveolin as a target in the prevention and treatment of diabetic cardiomyopathy.Frontiers in immunology · 2022Review
- Leucine imparts cardioprotective effects by enhancing mTOR activity and mitochondrial fusion in a myocardial ischemia/reperfusion injury murine model.Diabetology & metabolic syndrome · 2021Article
- Caveolin-3 is required for regulation of transient outward potassium current by angiotensin II in mouse atrial myocytes.American journal of physiology. Heart and circulatory physiology · 2021Article
- Whole-Exome Sequencing and hiPSC Cardiomyocyte Models IdentifyFrontiers in genetics · 2021Article
- Cardiac Connexin-43 Hemichannels and Pannexin1 Channels: Provocative Antiarrhythmic Targets.International journal of molecular sciences · 2020Review
- Caveolin as a Novel Potential Therapeutic Target in Cardiac and Vascular Diseases: A Mini Review.Aging and disease · 2020Review
- Protective role of cardiac-specific overexpression of caveolin-3 in cirrhotic cardiomyopathy.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Effect of type 2 diabetes mellitus caveolin-3 K15N mutation on glycometabolism.Experimental and therapeutic medicine · 2019Article
- Cardiac-Directed Expression of Adenylyl Cyclase Catalytic Domain (Human gene therapy · 2019Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
objectivesWe hypothesized that cardiac myocyte-specific overexpression of caveolin-3 (Cav-3), a muscle-specific caveolin, would alter natriuretic peptide signaling and attenuate cardiac hypertrophy.
backgroundNatriuretic peptides modulate cardiac hypertrophy and are potential therapeutic options for patients with heart failure. Caveolae, microdomains in the plasma membrane that contain caveolin proteins and natriuretic peptide receptors, have been implicated in cardiac hypertrophy and natriuretic peptide localization.
methodsWe generated transgenic mice with cardiac myocyte-specific overexpression of caveolin-3 (Cav-3 OE) and also used an adenoviral construct to increase Cav-3 in cardiac myocytes.
resultsThe Cav-3 OE mice subjected to transverse aortic constriction had increased survival, reduced cardiac hypertrophy, and maintenance of cardiac function compared with control mice. In left ventricle at baseline, messenger ribonucleic acid for atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were increased 7- and 3-fold, respectively, in Cav-3 OE mice compared with control subjects and were accompanied by increased protein expression for ANP and BNP. In addition, ventricles from Cav-3 OE mice had greater cyclic guanosine monophosphate levels, less nuclear factor of activated T-cell nuclear translocation, and more nuclear Akt phosphorylation than ventricles from control subjects. Cardiac myocytes incubated with Cav-3 adenovirus showed increased expression of Cav-3, ANP, and Akt phosphorylation. Incubation with methyl-β-cyclodextrin, which disrupts caveolae, or with wortmannin, a PI3K inhibitor, blocked the increase in ANP expression.
conclusionsThese results imply that cardiac myocyte-specific Cav-3 OE is a novel strategy to enhance natriuretic peptide expression, attenuate hypertrophy, and possibly exploit the therapeutic benefits of natriuretic peptides in cardiac hypertrophy and heart failure.
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