Mechanisms of non-apoptotic programmed cell death in diabetes and heart failure.
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.
Dorn
Gerald W
GW
Center for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA. gdorn@dom.wustl.edu
D000818:Animals; D017209:Apoptosis; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D006333:Heart Failure / Q000378:metabolism*; D018398:Homeodomain Proteins / Q000378:metabolism; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D051379:Mice; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000166:cytology / Q000378:metabolism; D009336:Necrosis / Q000378:metabolism*; D015398:Signal Transduction; D015534:Trans-Activators / Q000378:metabolism
D018398:Homeodomain Proteins; D008565:Membrane Proteins; D024101:Mitochondrial Proteins; C501741:Nix protein, mouse; D015534:Trans-Activators; C084010:pancreatic and duodenal homeobox 1 protein
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