Document Detail

Coping with Endoplasmic Reticulum Stress in the Cardiovascular System.
MedLine Citation:
PMID:  23020580     Owner:  NLM     Status:  Publisher    
The endoplasmic reticulum (ER) is a multifunctional intracellular organelle, a component of the cellular reticular network that allows cells to adjust to a wide variety of conditions. The cardiomyocyte reticular network is the ideal location of sensors for both intrinsic and extrinsic factors that disrupt energy and/or nutrient homeostasis and lead to ER stress, a disturbance in ER function. ER stress has been linked to both physiological and pathological states in the cardiovascular system; such states include myocardial infarction, oxygen starvation (hypoxia) and fuel starvation, ischemia, pressure overload, dilated cardiomyopathy, hypertrophy, and heart failure. The ER stress coping response (e.g., the unfolded protein response) is composed of discrete pathways that are controlled by a collection of common regulatory components that may function as a single entity involved in reacting to ER stress. These corrective strategies allow the cardiomyocyte reticular network to restore energy and/or nutrient homeostasis and to avoid cell death. Therefore, the identities of the ER stress corrective strategies are important targets for the development of therapeutic approaches for cardiovascular and other acquired disorders. Expected final online publication date for the Annual Review of Physiology Volume 75 is February 10, 2013. Please see for revised estimates.
Jody Groenendyk; Luis B Agellon; Marek Michalak
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-9-27
Journal Detail:
Title:  Annual review of physiology     Volume:  -     ISSN:  1545-1585     ISO Abbreviation:  Annu. Rev. Physiol.     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-10-1     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0370600     Medline TA:  Annu Rev Physiol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Department of Biochemistry, University of Alberta, Edmonton, Alberta, Canada T6G 2H7.
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