期刊
JOURNAL OF CELLULAR PHYSIOLOGY
卷 227, 期 5, 页码 1791-1795出版社
WILEY
DOI: 10.1002/jcp.22903
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资金
- Council of Scientific and Industrial Research [SIP006]
- Council of Scientific and Industrial Research (CSIR), New Delhi, India [SIP006]
Apoptosis or programmed cell death is an extremely coordinated phenomenon that involves the participation of a complex interacting crosstalk between the endoplasmic reticulum and mitochondria. This involves a series of signaling molecules like stress kinases, caspases, Bcl-2 family of proteins, etc. that coordinately induce apoptosis by releasing apoptotic proteins from the mitochondria and mediate DNA damage of the cell. Among the stress kinases, JNK, a member of the MAPK family has been believed to be critically mediating these apoptotic phenomena. The involvement of JNK has been clouded by controversies because of its role both as a pro-apoptotic and an anti-apoptotic mediator. A very significant initiator of JNK activation is the pro-inflammatory cytokine, IL-1 beta, levels of which are significantly elevated in varied diseases especially diabetes where it is believed to significantly contribute to pancreatic beta-cell death. During apoptotic cell death, the endoplasmic reticulum and the mitochondrion participate in a relay of cellular events that determine the onset of the classical apoptotic pathways. Here we discuss the details of this ER-mitochondrial crosstalk and the role of JNK herein that ultimately culminates into apoptotic cell death that is evident in various pathophysiological conditions. J. Cell. Physiol. 227: 1791-1795, 2012. (C) 2011 Wiley Periodicals, Inc.
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