title: Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress.
abstract: The ability to respond to perturbations in endoplasmic reticulum (ER) function is a fundamentally important property of all cells, but ER stress can also lead to apoptosis. In settings of chronic ER stress, the associated apoptosis may contribute to pathophysiological processes involved in a number of prevalent diseases, including neurodegenerative diseases, diabetes, atherosclerosis and renal disease. The molecular mechanisms linking ER stress to apoptosis are the topic of this review, with emphases on relevance to pathophysiology and integration and complementation among the various apoptotic pathways induced by ER stress.
authors.affiliation: Department of Medicine, Anatomy & Cell Biology, Columbia University, New York, NY 10032, USA. iat1@columbia.edu
authors.forename: Ira
authors.initials: I
authors.lastname: Tabas
authors.forename: David
authors.initials: D
authors.lastname: Ron
mesh_terms: D000818:Animals; D017209:Apoptosis; D002470:Cell Survival; D004195:Disease Models, Animal; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D006801:Humans; D008954:Models, Biological; D012333:RNA, Messenger / Q000378:metabolism; D017382:Reactive Oxygen Species; D051742:Transcription Factor CHOP / Q000378:metabolism; D056811:Unfolded Protein Response
chemical_list: D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D051742:Transcription Factor CHOP