Document Detail


Cardioprotective mechanisms activated in response to myocardial ischemia.
MedLine Citation:
PMID:  22338709     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
Myocardial ischemia, a disorder causing myocardial infarction and malfunction, can activate various adaptive mechanisms that protect cardiomyocytes from ischemic injury. During the early hours post myocardial ischemia, injured cardiac cells can release several molecules, including adenosine, opioids, and bradykinin, which promote myocardial survival by activating the G protein signaling pathways. During a later phase about several days, myocardial ischemia induces upregulation of growth factors and cytokines, including VEGF, ILGF, HGF, and SDF-1, in the injured myocardium, contributing to cardioprotection. In addition to the injured heart, the liver participates in cardioprotection. In response to myocardial ischemia, the liver upregulates and releases secretory proteins, including FGF21 and TFF3, both of which promote cardiomyocyte survival. The liver also provides a reservoir of hepatic cells that mobilize to the site of myocardial ischemia, potentially contributing to cardioprotection. Taken together, the early and late mechanisms act coordinately in a time-dependent manner, ensuring effective cardioprotection post myocardial infarction. Investigations on these innate cardioprotective mechanisms have provided insights into the development of cardioprotective strategies for treating myocardial infarction. In this article, the authors review the innate mechanisms of cardioprotection in myocardial ischemia.
Authors:
Shu Q Liu; Brandon J Tefft; Di Zhang; Derek Roberts; Daniel J Schuster; Allison Wu
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Molecular & cellular biomechanics : MCB     Volume:  8     ISSN:  1556-5297     ISO Abbreviation:  Mol Cell Biomech     Publication Date:  2011 Dec 
Date Detail:
Created Date:  2012-02-17     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101253756     Medline TA:  Mol Cell Biomech     Country:  United States    
Other Details:
Languages:  eng     Pagination:  319-38     Citation Subset:  IM    
Affiliation:
Biomedical Engineering Department, Northwestern University, Evanston, IL 60208-3107, USA. sliu@northwestern.edu
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