{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,30]],"date-time":"2025-11-30T13:35:34Z","timestamp":1764509734857,"version":"3.46.0"},"reference-count":46,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2025,8,7]],"date-time":"2025-08-07T00:00:00Z","timestamp":1754524800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Fundamemntal Clinical Pharma"],"published-print":{"date-parts":[[2025,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Cardiac hypertrophy often transits into heart failure. Angiogenesis significantly affects the pathogenesis of cardiac hypertrophy. Cytoplasmic integrin\u2010linked kinase (ILK) regulates cardiac angiogenesis by stimulating vascular endothelial growth factor (VEGF). There is a lack of evidence that investigates the effect of \u03b1\n                      <jats:sub>1A<\/jats:sub>\n                      \u2010adrenoceptor blockade on ILK\u2010related angiogenesis. Thus, the current study aims to examine the effect of tamsulosin on ILK\u2010related angiogenesis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Method<\/jats:title>\n                    <jats:p>Twenty\u2010four Wistar rats were divided into four groups as follows: control receiving 0.9% NaCl; an isoproterenol (ISO)\u2010treated (5\u2009mg\/kg\/day); tamsulosin\u2010treated (0.4\u2009mg\/kg\/day); and tamsulosin\u2009+\u2009ISO\u2013treated group. The cardiac injuries, angiogenic biomarkers, and target proteins expressions were assessed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Tamsulosin significantly attenuated the cardiac hypertrophy index and biomarkers. Tamsulosin reversed histopathological changes in cardiac tissues and mediated significant modulation in VEGF, eNOS, ILK, p\u2010PI3K, p\u2010Akt, Flt\u20101, and PECAM\u20101 expressions.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      The data indicate that targeting \u03b1\n                      <jats:sub>1A<\/jats:sub>\n                      adrenoceptors by inhibition offers a promising therapeutic approach for preventing cardiac hypertrophy via signal\u2010transduction pathways, including ILK\u2010related VEGF\/eNOS\/PI3K\/Akt.\n                    <\/jats:p>\n                  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