{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T20:28:50Z","timestamp":1786566530726,"version":"build-2736575974"},"reference-count":57,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T00:00:00Z","timestamp":1774569600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T00:00:00Z","timestamp":1774569600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biochem &amp;amp; Molecular Tox"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Mitochondrial and endothelial dysfunction play a crucial role in the progression of myocardial infarction(MI). In this study, we appraised the cardioprotective effects of cuminaldehyde, a monocyclic terpenoid, and its molecular mechanisms by analyzing novel peroxisome proliferator\u2010activated receptor\u2010gamma coactivator\u20101\u03b1(PGC\u20101\u03b1)\/NADH\u2010dehydrogenase 2 (ND2)\u2010mediated mitochondrial and endothelial nitric oxide synthase (eNOS)\/nitric oxide (NO)\/vascular cell adhesion molecule\u20101(VCAM\u20101) mediated endothelial dysfunction pathways in isoproterenol\u2010induced myocardial infarcted rats. MI was induced in rats by isoproterenol (100\u2009mg\/kg body weight). Then, cuminaldehyde (20\u2009mg\/kg body weight) was administered orally daily for 3 weeks, and parameters related to mitochondrial and endothelial dysfunction were evaluated. The findings of this study showed that after isoproterenol administration, serum cardiac sensitive markers and heart rate increased. Furthermore, lipid peroxidation products and calcium ions were elevated, whereas antioxidants, isocitrate dehydrogenase, malate dehydrogenase, \u03b1\u2010ketoglutarate dehydrogenase, NADH dehydrogenase, cytochrome c oxidase and adenosine triphosphate were decreased in isoproterenol\u2010induced heart mitochondria. The transmission electron microscopic study validated mitochondrial damage. RT\u2010PCR revealed reduced myocardial expression of PGC\u20101\u03b1 and ND2. Moreover, the MI group showed lowered plasma NO, and the ELISA study revealed reduced eNOS and enhanced VCAM\u20101 in serum. The myocardial eNOS expression was diminished, and myocardial VCAM\u20101 expression was increased by RT\u2010PCR. Histopathological findings revealed myocardial damage. Nevertheless, cuminaldehyde decreased cardiac diagnostic markers, heart rate, lipid peroxidation products, calcium ions, VCAM\u20101, and increased antioxidant system, mitochondrial enzymes, adenosine triphosphate, PGC\u20101\u03b1, ND2, NO, eNOS, and preserved mitochondrial and heart tissue architecture. Thus, cuminaldehyde modulated PGC\u20101\u03b1\/ND2 and eNOS\/NO\/VCAM\u20101 pathways and alleviated mitochondrial and endothelial dysfunction, thereby mitigating MI in isoproterenol\u2010induced rats and protecting the heart, by its anti\u2010mitochondrial and anti\u2010endothelial dysfunction mechanisms.<\/jats:p>","DOI":"10.1002\/jbt.70805","type":"journal-article","created":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T11:47:14Z","timestamp":1774612034000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Cardioprotective Effects of Cuminaldehyde Mitigate Isoproterenol\u2010Induced Myocardial Infarction by Modulating the PGC\u20101\u03b1\/ND2\u2010Mediated Mitochondrial and eNOS\/NO\/VCAM\u20101\u2010 Mediated Endothelial Dysfunction Pathways"],"prefix":"10.1002","volume":"40","author":[{"ORCID":"https:\/\/orcid.org\/0009-0009-0642-3569","authenticated-orcid":false,"given":"Shervin Prince","family":"Stanely","sequence":"first","affiliation":[{"name":"Division of Biotechnology, Karunya Institute of Technology and Sciences Deemed to be University Coimbatore Tamil Nadu South India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9996-0957","authenticated-orcid":false,"given":"Reya","family":"Issac","sequence":"additional","affiliation":[{"name":"Division of Biotechnology, Karunya Institute of Technology and Sciences Deemed to be University Coimbatore Tamil Nadu South India"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,3,27]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.biopha.2022.112775"},{"key":"e_1_2_10_3_1","first-page":"123","article-title":"Punicalagin Attenuates Isoproterenol\u2010Induced Myocardial Infarction Through Nuclear Factor Erythroid 2\u2010related Factor 2\/silent Information Regulator transcript\u20101\u2010mediated Inhibition of Inflammation and Cardiac Stress Markers in Experimental Animal Models","volume":"75","author":"Liao X. 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