Regular ArticleProgrammed Myocyte Cell Death Affects the Viable Myocardium after Infarction in Rats
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Effects of 17-AAG on the RIP1/RIP3/MLKL pathway during the development of heart failure following myocardial infarction in rats
2021, Journal of Pharmacological Sciences5-Methoxytryptophan attenuates postinfarct cardiac injury by controlling oxidative stress and immune activation
2021, Journal of Molecular and Cellular CardiologyCitation Excerpt :Apoptosis and inflammation following acute MI are critical pathophysiological processes that lead to cardiac remodeling and dysfunction [6]. Apoptosis of cardiomyocytes and nonmyocytes occurs in infarct and peri-infarct zones immediately after MI [7,8]. Excessive apoptosis can lead to progressive myocardial loss, fibrosis, and functional deterioration [9].
Effects of Hsp90 inhibitor on the RIP1-RIP3-MLKL pathway during the development of heart failure in mice
2021, European Journal of PharmacologyGenetic deletion of soluble epoxide hydrolase provides cardioprotective responses following myocardial infarction in aged mice
2017, Prostaglandins and Other Lipid MediatorsCitation Excerpt :Prolonged ischemia results in both necrotic and apoptotic cell death throughout the myocardium. Myocardial apoptosis has been shown to increase shortly after MI in both the infarcted and non-infarcted regions of the heart [47]. 20S proteasome activity is involved in regulating the cell death cascades through the cleavage of pro-death proteins and removal of proteins damaged by oxidative stress, mutation or misfolding [48].
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