Document Detail


PPAR-γ and AMPK - Advantageous targets for myocardial ischemia/reperfusion therapy.
MedLine Citation:
PMID:  21536015     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Ischemic heart disease stands as the number one leading cause of death in the United States. Current interventions rely on the immediate restoration of blood flow to the ischemic area; however, this in turn may trigger a series of undesirable events that are further injurious to the myocardium, termed ischemia/reperfusion (I/R) injury. Therefore, there is a need for novel therapeutic strategies aimed at limiting the extent of myocardial injury. Yet, the molecular mechanisms responsible for I/R injury remain largely indefinable. Research efforts are currently investigating various signaling mechanisms to be used for potential targets limiting cardiac injury due to such cardiovascular events. In this review, we highlight two potential molecular targets, PPAR-γ and AMPK, which have been extensively reported to have various cardioprotective capabilities against I/R injury. Although functionally different, the pathways these proteins mediate seem to intersect and possibly act synergistically potentiating a cardioprotective response.
Authors:
Alex Morrison; Ji Li
Related Documents :
11091805 - Management of unstable angina.
1222435 - Left ventricular pressure responses in post-angiographic angina.
1598865 - Immediate and follow-up results of the conservative coronary angioplasty strategy for u...
21098415 - A new agent for atrial fibrillation: electrophysiological properties of dronedarone.
17675905 - A triglyceride/high-density lipoprotein ratio > or = 3.5 is associated with an increase...
22783585 - The adoption of clinical pathways and the inclusion of likelihood ratios in the report:...
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-4-21
Journal Detail:
Title:  Biochemical pharmacology     Volume:  -     ISSN:  1873-2968     ISO Abbreviation:  -     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-5-3     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0101032     Medline TA:  Biochem Pharmacol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2011. Published by Elsevier Inc.
Affiliation:
Department of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, University at Buffalo-SUNY, 3435 Main Street, Buffalo, NY 14214, United States.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  The A391E mutation enhances FGFR3 activation in the absence of ligand.
Next Document:  Tert-butyl-2(4,5-dihydrogen-4,4,5,5-tetramethyl-3-O-1H-imidazole-3-cationic-1-oxyl-2-pyrrolidine-1-c...