ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Caveolin-1 deficiency exacerbates cardiac dysfunction and reduces survival in mice with myocardial infarction.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 51 citations in OpenAlex.
- Remodeling of the cardiac striatin interactome and its dynamics in the diabetic heart.Scientific reports · 2025Article
- Caveolin and oxidative stress in cardiac pathology.Frontiers in physiology · 2025Review
- Interplay between caveolin-1 and mineralocorticoid receptor in cardiometabolic disease.The Journal of endocrinology · 2024Review
- CAV1 Protein Encapsulated in Mouse BMSC-Derived Extracellular Vesicles Alleviates Myocardial Fibrosis Following Myocardial Infarction by Blocking the TGF-β1/SMAD2/c-JUN Axis.Journal of cardiovascular translational research · 2024Article
- The purified extract of steamedJournal of ginseng research · 2023Article
- The importance of caveolin as a target in the prevention and treatment of diabetic cardiomyopathy.Frontiers in immunology · 2022Review
- CAV-1 Overexpression Exacerbates the Manifestation in EPAC-1-Induced Chronic Postsurgical Pain in Rats.Pain research & management · 2022Article
- Loss of Caveolin-1 and caveolae leads to increased cardiac cell stiffness and functional decline of the adult zebrafish heart.Scientific reports · 2020Article
- Therapeutic Angiogenesis with Sound Waves.Annals of vascular diseases · 2020Article
- Caveolin as a Novel Potential Therapeutic Target in Cardiac and Vascular Diseases: A Mini Review.Aging and disease · 2020Review
- Role of Caveolin-1 in Diabetes and Its Complications.Oxidative medicine and cellular longevity · 2020Review
- Buyang Huanwu Decoction Exerts Cardioprotective Effects through Targeting Angiogenesis via Caveolin-1/VEGF Signaling Pathway in Mice with Acute Myocardial Infarction.Oxidative medicine and cellular longevity · 2019Article
- Caveolin-1 and MLRs: A potential target for neuronal growth and neuroplasticity after ischemic stroke.International journal of medical sciences · 2019Review
- Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection.Cardiovascular diabetology · 2017Review
- Phosphorylated CAV1 activates autophagy through an interaction with BECN1 under oxidative stress.Cell death & disease · 2017Article
- Reversal of maladaptive fibrosis and compromised ventricular function in the pressure overloaded heart by a caveolin-1 surrogate peptide.Laboratory investigation; a journal of technical methods and pathology · 2017Article
- Modulation of caveolins, integrins and plasma membrane repair proteins in anthracycline-induced heart failure in rabbits.PloS one · 2017Article
- Differential roles of caveolin-1 in ouabain-induced Na+/K+-ATPase cardiac signaling and contractility.Physiological genomics · 2016Article
- Article
- Systems analysis of gene ontology and biological pathways involved in post-myocardial infarction responses.BMC genomics · 2015Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
Caveolin (Cav)-1 has been involved in the pathogenesis of ischemic injuries. For instance, modulations of Cav-1 expression have been reported in animal models of myocardial infarction and cerebral ischemia-reperfusion. Furthermore, ablation of the Cav-1 gene in mice has been shown to increase the extent of ischemic injury in models of cerebral and hindlimb ischemia. Cav-1 has also been suggested to play a role in myocardial ischemic preconditioning. However, the role of Cav-1 in myocardial ischemia (MI)-induced cardiac dysfunction still remains to be determined. We determined the outcome of a permanent left anterior descending coronary artery (LAD) ligation in Cav-1 knockout (KO) mice. Wild-type (WT) and Cav-1 KO mice were subjected to permanent LAD ligation for 24 h. The progression of ischemic injury was monitored by echocardiography, hemodynamic measurements, 2,3,5-triphenyltetrazolium chloride staining, β-binding analysis, cAMP level measurements, and Western blot analyses. Cav-1 KO mice subjected to LAD ligation display reduced survival compared with WT mice. Despite similar infarct sizes, Cav-1 KO mice subjected to MI showed reduced left ventricular (LV) ejection fraction and fractional shortening as well as increased LV end-diastolic pressures compared with their WT counterparts. Mechanistically, Cav-1 KO mice subjected to MI exhibit reduced β-adrenergic receptor density at the plasma membrane as well as decreased cAMP levels and PKA phosphorylation. In conclusion, ablation of the Cav-1 gene exacerbates cardiac dysfunction and reduces survival in mice subjected to MI. Mechanistically, Cav-1 KO mice subjected to LAD ligation display abnormalities in β-adrenergic signaling.
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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.