Journal
CARDIOVASCULAR DRUGS AND THERAPY
Volume 20, Issue 6, Pages 445-462Publisher
SPRINGER
DOI: 10.1007/s10557-006-0583-7
Keywords
apoptosis; autophagy; mitochondria; GFP-LC3
Funding
- NHLBI NIH HHS [R01-HL60590] Funding Source: Medline
- NIA NIH HHS [R01-AG21568] Funding Source: Medline
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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.
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