TY - JOUR
T1 - Cardiomyocyte death
T2 - Mechanisms and translational implications
AU - Chiong, M.
AU - Wang, Z. V.
AU - Pedrozo, Z.
AU - Cao, D. J.
AU - Troncoso, R.
AU - Ibacache, M.
AU - Criollo, A.
AU - Nemchenko, A.
AU - Hill, J. A.
AU - Lavandero, S.
N1 - Funding Information:
Acknowledgements. We thank the members from the Hill lab and Lavandero lab for helpful discussions. This work was supported by grants from the NIH (HL-075173, JAH; HL-080144, JAH; and HL-090842, JAH), AHA (0640084N, JAH), the AHA-Jon Holden DeHaan Foundation (0970518N, JAH), and the Fondo Nacional de Desarrollo Cientifico y Tecnologico: FONDECYT 1080436 and FONDAP 15010006 (SL). ZVW, ZP, and RT are supported by postdoctoral fellowships from the American Heart Association 10POST4320009 and FONDECYT 3110039 and 3110114, respectively.
PY - 2011/12
Y1 - 2011/12
N2 - Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide. Although treatments have improved, development of novel therapies for patients with CVD remains a major research goal. Apoptosis, necrosis, and autophagy occur in cardiac myocytes, and both gradual and acute cell death are hallmarks of cardiac pathology, including heart failure, myocardial infarction, and ischemia/reperfusion. Pharmacological and genetic inhibition of autophagy, apoptosis, or necrosis diminishes infarct size and improves cardiac function in these disorders. Here, we review recent progress in the fields of autophagy, apoptosis, and necrosis. In addition, we highlight the involvement of these mechanisms in cardiac pathology and discuss potential translational implications.
AB - Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide. Although treatments have improved, development of novel therapies for patients with CVD remains a major research goal. Apoptosis, necrosis, and autophagy occur in cardiac myocytes, and both gradual and acute cell death are hallmarks of cardiac pathology, including heart failure, myocardial infarction, and ischemia/reperfusion. Pharmacological and genetic inhibition of autophagy, apoptosis, or necrosis diminishes infarct size and improves cardiac function in these disorders. Here, we review recent progress in the fields of autophagy, apoptosis, and necrosis. In addition, we highlight the involvement of these mechanisms in cardiac pathology and discuss potential translational implications.
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U2 - 10.1038/cddis.2011.130
DO - 10.1038/cddis.2011.130
M3 - Review article
C2 - 22190003
AN - SCOPUS:84862908305
SN - 2041-4889
VL - 2
JO - Cell Death and Disease
JF - Cell Death and Disease
IS - 12
M1 - e244
ER -