{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T20:08:01Z","timestamp":1789848481800,"version":"4.0.1"},"reference-count":24,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,1,29]],"date-time":"2026-01-29T00:00:00Z","timestamp":1769644800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,29]],"date-time":"2026-01-29T00:00:00Z","timestamp":1769644800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Acute myocardial infarction (MI) accelerates cardiomyocyte apoptosis, which underpins ventricular remodelling and dysfunction. The hormone ghrelin mitigates this remodelling, but the mechanisms remain unclear. Specific microRNAs (miRs) are key modulators and reliable biomarkers of early\u2010stage apoptosis. We hypothesized that ghrelin targets anti\u2010apoptotic miR\u2010499 and miR\u2010133 following MI to suppress cardiac apoptosis and thus mitigate cardiac dysfunction. C57\/B6 mice received an injection of ghrelin (150\u00a0\u00b5g\/kg,\n                    <jats:sc>s.c.<\/jats:sc>\n                    ) or saline following left anterior descending coronary artery ligation (MI). Plasma levels of miR\u2010499 and miR\u2010133 at 3 or 24\u00a0h post\u2010MI were measured using real\u2010time PCR. Echocardiography and TUNEL staining were used to assess progressive cardiac function\/structure and cardiomyocyte apoptosis, respectively. Myocardial ischaemia adversely decreased the levels of anti\u2010apoptotic miR\u2010499 by 3\u00a0h post\u2010MI and increased the proportion of TUNEL\u2010positive apoptotic cardiomyocytes by 24\u00a0h post\u2010MI, contributing to cardiac remodelling and dysfunction by 2 weeks post\u2010MI. Ghrelin prevented this MI\u2010induced decrease in miR\u2010499 by 3\u00a0h post\u2010MI, then further increased the levels of miR\u2010499 and miR\u2010133 by 24\u00a0h. These ghrelin\u2010mediated changes in microRNA were associated with a significant decrease in cardiomyocyte apoptosis and, consequently, significantly improved cardiac function and structure by 2\u00a0weeks post\u2010MI. These results highlight miRs as effective biomarkers for the early detection of ischaemia\u2010induced apoptotic signalling. Moreover, ghrelin appears to mitigate ischaemia\u2010induced apoptosis by increasing the levels of anti\u2010apoptotic miR\u2010499 and miR\u2010133, further solidifying ghrelin as a new therapeutic strategy for the clinical treatment of heart failure.\n                  <\/jats:p>","DOI":"10.1113\/ep093314","type":"journal-article","created":{"date-parts":[[2026,1,29]],"date-time":"2026-01-29T20:38:32Z","timestamp":1769719112000},"page":"1618-1625","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Ghrelin protects against cell death in myocardial ischaemia: Emerging role of microRNA"],"prefix":"10.1113","volume":"111","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5419-7935","authenticated-orcid":false,"given":"Rajesh","family":"Katare","sequence":"first","affiliation":[{"name":"Department of Physiology, School of Biomedical Sciences University of Otago  Dunedin New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey R.","family":"Erickson","sequence":"additional","affiliation":[{"name":"Department of Physiology, School of Biomedical Sciences University of Otago  Dunedin New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4506-2948","authenticated-orcid":false,"given":"Daryl O.","family":"Schwenke","sequence":"additional","affiliation":[{"name":"Department of Physiology, School of Biomedical Sciences University of Otago  Dunedin New 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