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dc.contributor.authorKannaporn Intachaien_US
dc.contributor.authorSiriporn C. Chattipakornen_US
dc.contributor.authorNipon Chattipakornen_US
dc.contributor.authorKrekwit Shinlapawittayatornen_US
dc.date.accessioned2018-11-29T07:32:32Z-
dc.date.available2018-11-29T07:32:32Z-
dc.date.issued2018-09-01en_US
dc.identifier.issn14220067en_US
dc.identifier.issn16616596en_US
dc.identifier.other2-s2.0-85052527249en_US
dc.identifier.other10.3390/ijms19092466en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85052527249&origin=inwarden_US
dc.identifier.urihttp://cmuir.cmu.ac.th/jspui/handle/6653943832/62565-
dc.description.abstract© 2018 by the authors. Licensee MDPI, Basel, Switzerland. Acute myocardial infarction (AMI) is the most common cause of acute myocardial injury and its most clinically significant form. The most effective treatment for AMI is to restore an adequate coronary blood flow to the ischemic myocardium as quickly as possible. However, reperfusion of an ischemic region can induce cardiomyocyte death, a phenomenon termed “myocardial ischemia/reperfusion (I/R) injury”. Disruption of cardiac parasympathetic (vagal) activity is a common hallmark of a variety of cardiovascular diseases including AMI. Experimental studies have shown that increased vagal activity exerts cardioprotective effects against myocardial I/R injury. In addition, acetylcholine (ACh), the principle cardiac vagal neurotransmitter, has been shown to replicate the cardioprotective effects of cardiac ischemic conditioning. Moreover, studies have shown that cardiomyocytes can synthesize and secrete ACh, which gives further evidence concerning the importance of the non-neuronal cholinergic signaling cascades. This suggests that the activation of ACh receptors is involved in cardioprotection against myocardial I/R injury. There are two types of ACh receptors (AChRs), namely muscarinic and nicotinic receptors (mAChRs and nAChRs, respectively). However, the effects of AChRs activation in cardioprotection during myocardial I/R are still not fully understood. In this review, we summarize the evidence suggesting the association between AChRs activation with both electrical and pharmacological interventions and the cardioprotection during myocardial I/R, as well as outline potential mechanisms underlying these cardioprotective effects.en_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.subjectChemical Engineeringen_US
dc.subjectChemistryen_US
dc.subjectComputer Scienceen_US
dc.titleRevisiting the cardioprotective effects of acetylcholine receptor activation against myocardial ischemia/reperfusion injuryen_US
dc.typeJournalen_US
article.title.sourcetitleInternational Journal of Molecular Sciencesen_US
article.volume19en_US
article.stream.affiliationsChiang Mai Universityen_US
Appears in Collections:CMUL: Journal Articles

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