{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T16:45:12Z","timestamp":1773420312238,"version":"3.50.1"},"reference-count":39,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2011,4]]},"abstract":"<jats:p>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, \u03b2-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 \u03b2-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 \u03b2-adrenergic signaling.<\/jats:p>","DOI":"10.1152\/ajpheart.01173.2010","type":"journal-article","created":{"date-parts":[[2011,2,5]],"date-time":"2011-02-05T05:16:18Z","timestamp":1296882978000},"page":"H1274-H1281","source":"Crossref","is-referenced-by-count":41,"title":["Caveolin-1 deficiency exacerbates cardiac dysfunction and reduces survival in mice with myocardial infarction"],"prefix":"10.1152","volume":"300","author":[{"given":"Jean-Fran\u00e7ois","family":"Jasmin","sequence":"first","affiliation":[{"name":"Department of Stem Cell Biology and Regenerative Medicine,"},{"name":"The Jefferson Stem Cell Biology and Regenerative Medicine Center, and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Giuseppe","family":"Rengo","sequence":"additional","affiliation":[{"name":"Center for Translational Medicine and the George Zallie and Family Laboratory for Cardiovascular Gene Therapy, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania;"},{"name":"Division of Cardiology, \u201cSalvatore Maugeri\u201d Foundation, IRCCS, Telese Terme, Italy;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anastasios","family":"Lymperopoulos","sequence":"additional","affiliation":[{"name":"Center for Translational Medicine and the George Zallie and Family Laboratory for Cardiovascular Gene Therapy, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania;"},{"name":"Department of Pharmaceutical Sciences, College of Pharmacy, Nova Southeastern University, Fort Lauderdale, Florida;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ratika","family":"Gupta","sequence":"additional","affiliation":[{"name":"Department of Stem Cell Biology and Regenerative Medicine,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gregory J.","family":"Eaton","sequence":"additional","affiliation":[{"name":"Department of Stem Cell Biology and Regenerative Medicine,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kevin","family":"Quann","sequence":"additional","affiliation":[{"name":"Department of Stem Cell Biology and Regenerative Medicine,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Donna M.","family":"Gonzales","sequence":"additional","affiliation":[{"name":"Department of Stem Cell Biology and Regenerative Medicine,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Isabelle","family":"Mercier","sequence":"additional","affiliation":[{"name":"Department of Stem Cell Biology and Regenerative Medicine,"},{"name":"The Jefferson Stem Cell Biology and Regenerative Medicine Center, and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Walter J.","family":"Koch","sequence":"additional","affiliation":[{"name":"Center for Translational Medicine and the George Zallie and Family Laboratory for Cardiovascular Gene Therapy, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael P.","family":"Lisanti","sequence":"additional","affiliation":[{"name":"Department of Stem Cell Biology and Regenerative Medicine,"},{"name":"The Jefferson Stem Cell Biology and Regenerative Medicine Center, and"},{"name":"Departments of Medical Oncology, and Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania; 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