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Nicorandil Protects the Heart from Ischemia/Reperfusion Injury by Attenuating Endoplasmic Reticulum Response-induced Apoptosis Through PI3K/Akt Signaling Pathway
Author(s) -
Hui Wu,
Ming Ye,
H. J. Yang,
Jiawang Ding,
Jian Yang,
Wusong Dong,
Xinan Wang
Publication year - 2015
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000374035
Subject(s) - wortmannin , nicorandil , unfolded protein response , cardioprotection , endoplasmic reticulum , pi3k/akt/mtor pathway , protein kinase b , pharmacology , medicine , tunicamycin , apoptosis , reperfusion injury , endocrinology , chemistry , ischemia , microbiology and biotechnology , biology , biochemistry
As a vasodilatory drug used to treat angina, nicorandil has been shown to induce an infarct-limiting effect in various experimental animal models of myocardial ischemia-reperfusion (IR). There are multiple mechanisms causing the IR injury, among which, the endoplasmic reticulum (ER) stress and ER stress-initiated apoptosis are implicated to play an important role. However, whether ER stress is involved in nicorandil-induced cardioprotection is unknown.

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