Journal ArticleDOI
Cell Death in the Pathogenesis of Heart Disease: Mechanisms and Significance
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TLDR
Pharmacological and genetic inhibition of apoptosis and necrosis lessens infarct size and improves cardiac function in these disorders and a better understanding of these processes and their interrelationships may allow for the development of novel therapies for the major heart syndromes.Abstract:
Cell death was once viewed as unregulated. It is now clear that at least a portion of cell death is a regulated cell suicide process. This type of death can exhibit multiple morphologies. One of these, apoptosis, has long been recognized to be actively mediated, and many of its underlying mechanisms have been elucidated. Moreover, necrosis, the traditional example of unregulated cell death, is also regulated in some instances. Autophagy is usually a survival mechanism but can occur in association with cell death. Little is known, however, about how autophagic cells die. Apoptosis, necrosis, and autophagy occur in cardiac myocytes during myocardial infarction, ischemia/reperfusion, and heart failure. Pharmacological and genetic inhibition of apoptosis and necrosis lessens infarct size and improves cardiac function in these disorders. The roles of autophagy in ischemia/reperfusion and heart failure are unresolved. A better understanding of these processes and their interrelationships may allow for the development of novel therapies for the major heart syndromes.read more
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Effects and mechanisms of QiShenYiQi pills and major ingredients on myocardial microcirculatory disturbance, cardiac injury and fibrosis induced by ischemia-reperfusion.
TL;DR: Investigation in the past decade in the laboratory as well as in other's demonstrated the cardioprotection potential of QiShenYiQi Pills (QSYQ) and ingredients in experimental animal models of I/R injury, and results have offered insight into the mechanism thereby QSYQ prevents against cardiac I-R injury in clinic.
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Nuclear localization of the mitochondrial factor HIGD1A during metabolic stress.
Kurosh Ameri,Anthony M. Rajah,Vien Nguyen,Timothy A. Sanders,Arman Jahangiri,Michael DeLay,Matthew Donne,Hwa J. Choi,Kathryn V. Tormos,Yerem Yeghiazarians,Stefanie S. Jeffrey,Paolo Rinaudo,David H. Rowitch,Manish K. Aghi,Emin Maltepe +14 more
TL;DR: A novel nuclear localization of HIGD1A is demonstrated that is commonly observed in human disease processes in vivo, frequently observed in diverse pathological states such as myocardial infarction, hypoxic-ischemic encephalopathy (HIE), and different types of cancer.
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MicroRNA-140 attenuates myocardial ischemia-reperfusion injury through suppressing mitochondria-mediated apoptosis by targeting YES1.
TL;DR: Overexpression of miR‐140 could reduce the increase related to myocardian I/R injury in infarct size and myocardial enzymes, and it also could inhibit the expression of proteins related to mitochondrial morphology and myCardial I/ R‐induced mitochondrial apoptosis by targeting YES1.
Journal ArticleDOI
Palmitoyl acyltransferase Aph2 in cardiac function and the development of cardiomyopathy
Tielin Zhou,Jing Li,Peiquan Zhao,Huijuan Liu,Deyong Jia,Hao Jia,Lin He,Yong Cang,Yong Cang,Sharon Boast,Sharon Boast,Yi-Han Chen,Helene Thibault,Marielle Scherrer-Crosbie,Stephen P. Goff,Baojie Li,Baojie Li +16 more
TL;DR: These findings establish Aph2 as a critical in vivo regulator of cardiac function and reveal roles for protein palmitoylation in the development of other organs including eyes.
Journal ArticleDOI
Thyroid hormones improve cardiac function and decrease expression of pro-apoptotic proteins in the heart of rats 14 days after infarction.
Alexandre Luz de Castro,Rafael Oliveira Fernandes,Vanessa Duarte Ortiz,Cristina Campos,Jéssica Hellen Poletto Bonetto,Tânia R.G. Fernandes,Adriana Conzatti,Rafaela Siqueira,Angela Maria Vicente Tavares,Paulo Cavalheiro Schenkel,Adriane Belló-Klein,Alex Sander da Rosa Araujo +11 more
TL;DR: TH administration prevented the loss of ventricular wall thickness and improved cardiac function in the infarcted rats 14 days after the injury, and decreased the expression of pro-apoptotic proteins 14 days after myocardial infarction.
References
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