TY - JOUR
T1 - The interplay between pro-death and pro-survival signaling pathways in myocardial ischemia/reperfusion injury
T2 - Apoptosis meets autophagy
AU - Hamacher-Brady, Anne
AU - Brady, Nathan Ryan
AU - Gottlieb, Roberta Anne
N1 - Funding Information:
This work was supported by NIH grants R01-AG21568 and R01-HL60590 (to R.A.G.) and the Stein endowment fund. This is MS# 18245 of The Scripps Research Institute.
PY - 2006/12
Y1 - 2006/12
N2 - Introduction: Programmed cell death of cardiac myocytes occurs following a bout of ischemia/reperfusion (I/R), which results in reduced function of the heart. Numerous studies, including in vivo, have shown that cell death occurs via necrosis and apoptosis following I/R. Recently, autophagy has emerged as a powerful mediator of programmed cell death, either opposing or enhancing apoptosis, or acting as an alternative form of programmed cell death distinct from apoptosis. Aim: Here we review the apoptotic and autophagic signaling pathways, their influences on each other, and we discuss the relevance of autophagy in the heart.
AB - Introduction: Programmed cell death of cardiac myocytes occurs following a bout of ischemia/reperfusion (I/R), which results in reduced function of the heart. Numerous studies, including in vivo, have shown that cell death occurs via necrosis and apoptosis following I/R. Recently, autophagy has emerged as a powerful mediator of programmed cell death, either opposing or enhancing apoptosis, or acting as an alternative form of programmed cell death distinct from apoptosis. Aim: Here we review the apoptotic and autophagic signaling pathways, their influences on each other, and we discuss the relevance of autophagy in the heart.
KW - Apoptosis
KW - Autophagy
KW - GFP-LC3
KW - Mitochondria
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U2 - 10.1007/s10557-006-0583-7
DO - 10.1007/s10557-006-0583-7
M3 - Review article
C2 - 17149555
AN - SCOPUS:33846531305
SN - 0920-3206
VL - 20
SP - 445
EP - 462
JO - Cardiovascular Drugs and Therapy
JF - Cardiovascular Drugs and Therapy
IS - 6
ER -