{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,7]],"date-time":"2026-01-07T22:52:23Z","timestamp":1767826343985,"version":"3.49.0"},"reference-count":76,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2021,4,17]],"date-time":"2021-04-17T00:00:00Z","timestamp":1618617600000},"content-version":"vor","delay-in-days":106,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Fondo Ricerca Locale"},{"name":"Fondo Finanziamento delle Attivit\u00e0 Base di Ricerca"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:p>Endothelial cell injury and vascular function strongly correlate with cardiac function following ischemia\/reperfusion injury. Several studies indicate that endothelial cells are more sensitive to ischemia\/reperfusion compared to cardiomyocytes and are critical mediators of cardiac ischemia\/reperfusion injury. H<jats:sub>2<\/jats:sub>S is involved in the regulation of cardiovascular system homeostasis and can act as a cytoprotectant during ischemia\/reperfusion. Activation of ERK1\/2 in endothelial cells after H<jats:sub>2<\/jats:sub>S stimulation exerts an enhancement of angiogenesis while its inhibition significantly decreases H<jats:sub>2<\/jats:sub>S cardioprotective effects. In this work, we investigated how H<jats:sub>2<\/jats:sub>S pretreatment for 24 hours prevents the ischemia\/reperfusion injury and promotes angiogenesis on microvascular endothelial cells following an ischemia\/reperfusion protocol in vitro, using a hypoxic chamber and ischemic buffer to simulate the ischemic event. H<jats:sub>2<\/jats:sub>S preconditioning positively affected cell viability and significantly increased endothelial cell migration when treated with 1\u2009<jats:italic>\u03bc<\/jats:italic>M H<jats:sub>2<\/jats:sub>S. Furthermore, mitochondrial function was preserved when cells were preconditioned. Since ERK1\/2 phosphorylation was extremely enhanced in ischemia\/reperfusion condition, we inhibited ERK both directly and indirectly to verify how H<jats:sub>2<\/jats:sub>S triggers this pathway in endothelial cells. Taken together, our data suggest that H<jats:sub>2<\/jats:sub>S treatment 24 hours before the ischemic insult protects endothelial cells from ischemia\/reperfusion injury and eventually decreases myocardial injury.<\/jats:p>","DOI":"10.1155\/2021\/8886666","type":"journal-article","created":{"date-parts":[[2021,4,17]],"date-time":"2021-04-17T14:50:05Z","timestamp":1618671005000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["H<sub>2<\/sub>S Pretreatment Is Promigratory and Decreases Ischemia\/Reperfusion Injury in Human Microvascular Endothelial 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