Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 304, Issue 3, Pages 463-470Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/S0006-291X(03)00618-1
Keywords
mitochondrial permeability transition; hepatocytes; ischemia/reperfusion; necrosis; apoptosis
Categories
Ask authors/readers for more resources
Opening of high conductance permeability transition pores in mitochondria initiates onset of the mitochondrial permeability transition (NIPT). The NIPT is a causative event, leading to necrosis and apoptosis in hepatocytes after oxidative stress, Ca2+ toxicity. and ischemia/reperfusion. Cyclosporin A blocks opening of permeability transition pores and protects Cell death after these stresses. In contrast to necrotic cell death which is a consequence of ATP depletion, ATP is required for the development of apoptosis. Reperfusion and the return of normal pH after ischemia initiate the MPT, but the balance between ATP depletion after the MPT and ATP generation by glycolysis determines whether the fate of cells will be apoptotic or necrotic death. Thus, the MPT is a common pathway leading to both necrotic and apoptotic cell death after ischemia/reperfusion. (C) 2003 Elsevier Science (USA). All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available