Journal
ONCOGENE
Volume 27, Issue 50, Pages 6407-6418Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2008.308
Keywords
cell death; Bcl-2; endoplasmic reticulum; autophagy; mitochondria-associated membranes (MAM)
Funding
- Italian Association for Cancer Research (AIRC), Telethon
- University of Ferrara
- Italian University Ministry
- Emilia Romagna Region
- Italian Space Agency (ASI)
- NIH [1P01AG025532-01A1]
- United Mitochondrial Disease Foundation (UMDF)
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There is a growing consensus that the various forms of cell death ( necrosis, apoptosis and autophagy) are not separated by strict boundaries, but rather share molecular effectors and signaling routes. Among the latter, a clear role is played by calcium (Ca2+), the ubiquitous second messenger involved in the control of a broad variety of physiological events. Fine tuning of intracellular Ca2+ homeostasis by anti- and proapoptotic proteins shapes the Ca2+ signal to which mitochondria and other cellular effectors are exposed, and hence the efficiency of various cell death inducers. Here, we will review: (i) the evidence linking calcium homeostasis to the regulation of apoptotic, and more recently autophagic cell death, (ii) the discussion of mitochondria as a critical, although not unique checkpoint and (iii) the molecular and functional elucidation of ER/mitochondria contacts, corresponding to the mitochondria-associated membrane (MAM) subfraction and proposed to be a specialized signaling microdomain.
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