NDLI: The divergent roles of autophagy in ischemia and preconditioning.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Sheng, Rui Qin, Zheng-hong
Description	Country affiliation: China Author Affiliation: Sheng R ( Department of Pharmacology and Laboratory of Aging and Nervous Diseases, Soochow University School of Pharmaceutical Science, Suzhou 215123, China.); Qin ZH ( Department of Pharmacology and Laboratory of Aging and Nervous Diseases, Soochow University School of Pharmaceutical Science, Suzhou 215123, China.)
Abstract	Autophagy is an evolutionarily conserved and lysosome-dependent process for degrading and recycling cellular constituents. Autophagy is activated following an ischemic insult or preconditioning, but it may exert dual roles in cell death or survival during these two processes. Preconditioning or lethal ischemia may trigger autophagy via multiple signaling pathways involving endoplasmic reticulum (ER) stress, AMPK/TSC/mTOR, Beclin 1/BNIP3/SPK2, and FoxO/NF-κB transcription factors, etc. Autophagy then interacts with apoptotic and necrotic signaling pathways to regulate cell death. Autophagy may also maintain cell function by removing protein aggregates or damaged mitochondria. To date, the dual roles of autophagy in ischemia and preconditioning have not been fully clarified. The purpose of the present review is to summarize the recent progress in the mechanisms underlying autophagy activation during ischemia and preconditioning. A better understanding of the dual effects of autophagy in ischemia and preconditioning could help to develop new strategies for the preventive treatment of ischemia.
File Format	HTM / HTML
ISSN	16714083
e-ISSN	17457254
DOI	10.1038/aps.2014.151
Journal	Acta Pharmacologica Sinica
Issue Number	4
Volume Number	36
Language	English
Publisher	Macmillan Publishers Limited
Publisher Date	2015-04-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Pharmacology Autophagy Ischemia Metabolism Ischemic Preconditioning Signal Transduction Animals Endoplasmic Reticulum Stress Pathology Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Pharmacology Pharmacology (medical)

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