{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,3]],"date-time":"2025-07-03T04:15:59Z","timestamp":1751516159265,"version":"3.41.0"},"reference-count":36,"publisher":"Canadian Science Publishing","issue":"4","license":[{"start":{"date-parts":[[2020,8,1]],"date-time":"2020-08-01T00:00:00Z","timestamp":1596240000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":["cdnsciencepub.com"],"crossmark-restriction":false},"short-container-title":["Biochem. Cell Biol."],"published-print":{"date-parts":[[2020,8]]},"abstract":"<jats:p> Brain-type glycogen phosphorylase (pygb) is one of the rate-limiting enzymes in glycogenolysis that plays a crucial role in the pathogenesis of type 2 diabetes mellitus. Here we investigated the role of pygb in high-glucose (HG)-induced cardiomyocyte apoptosis and explored the underlying mechanisms, by using the specific pygb inhibitors or pygb siRNA. Our results show that inhibition of pygb significantly attenuates cell apoptosis and oxidative stress induced by HG in H9c2 cardiomyocytes. Inhibition of pygb improved glucose metabolism in cardiacmyocytes, as evidenced by increased glycogen content, glucose consumption, and glucose transport. Mechanistically, pygb inhibition activates the Akt\u2013GSK-3\u03b2 signaling pathway and suppresses the activation of NF-\u03baB in H9c2 cells exposed to HG. Additionally, pygb inhibition promotes the expression and the translocation of hypoxia-inducible factor-1\u03b1 (HIF-1\u03b1) after HG stimulation. However, the changes in glucose metabolism and HIF-1\u03b1 activation mediated by pygb inhibition are significantly reversed in the presence of the Akt inhibitor MK2206. In conclusion, this study found that inhibition of pygb prevents HG-induced cardiomyocyte apoptosis via activation of Akt\u2013HIF-\u03b1. <\/jats:p>","DOI":"10.1139\/bcb-2019-0247","type":"journal-article","created":{"date-parts":[[2020,1,6]],"date-time":"2020-01-06T21:34:15Z","timestamp":1578346455000},"page":"458-465","update-policy":"https:\/\/doi.org\/10.1139\/csp-crossmark-policy","source":"Crossref","is-referenced-by-count":5,"title":["Inhibition of brain-type glycogen phosphorylase ameliorates high glucose-induced cardiomyocyte apoptosis via Akt\u2013HIF-1\u03b1 activation"],"prefix":"10.1139","volume":"98","author":[{"given":"Xuehan","family":"Wu","sequence":"first","affiliation":[{"name":"The National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, 1299 Xuefu Avenue, Nanchang 330031, P.R. 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