Journal
CELL CYCLE
Volume 9, Issue 17, Pages 3442-3448Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.9.17.12944
Keywords
apoptosis; necrosis; mitochondrial permeability transition pore
Categories
Funding
- NHLBI NIH HHS [R01 HL059888] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL059888] Funding Source: NIH RePORTER
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Programmed cell elimination is an important pathological mediator of disease. Multiple pathways to programmed cell death have been delineated, including apoptosis, autophagy and programmed necrosis. Cross-talk between the signaling pathways mediating each process has made it difficult to define specific mechanisms of in vivo programmed cell death. For this reason, many apoptotic diseases may involve other death signaling pathways. Recent advances in genetic complementation using mouse knock-out models are helping to dissect apoptotic and necrotic cell death in different pathological states. The current state of research in this area is reviewed, focusing upon new findings describing the role of programmed necrosis induced by the mitochondrial permeability transition in mouse models of heart failure and diabetes.
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