Document Detail


The role of PPAR in myocardial response to ischemia in normal and diseased heart.
MedLine Citation:
PMID:  22131314     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Peroxisome proliferator-activated receptors (PPAR), ligand-activated transcription factors, belong to the nuclear hormone receptor superfamily regulating expression of genes involved in different aspects of lipid metabolism, inflammation and cardiac energy production. Activation of PPAR-α isoform by its natural ligands, fatty acids (FA) and eicosanoids, promotes mitochondrial FA oxidation as the primary ATP-generating pathway. On the other hand, PPAR-γ regulates lipid anabolism or storage, while, until recently, the function of PPAR-β/δ has been less explored. Under conditions associated with acute or chronic oxygen deprivation, PPAR-α modulates expression of genes that determine substrate switch (FA vs. glucose) aimed at maintenance of basic cardiac function. Although PPAR-α and PPAR-γ synthetic agonists, hypolipidemic and antidiabetic drugs, have been reported to protect the heart against ischemia/reperfusion injury, it is still a matter of debate whether PPAR activation plays a beneficial or detrimental role in myocardial response to ischemia, in particular, in pathological conditions. This article reviews some findings demonstrating the impact of PPAR activation on cardiac resistance to ischemia in normal and pathologically altered heart. Specifically, it addresses the issue of susceptibility to ischemia in the diabetic myocardium, with particular regards to the role of PPAR. Finally, involvement of PPAR in the mechanisms of lipid-independent cardioprotective effects of some hypolipidemic drugs is also discussed.
Authors:
Tana Ravingerova; Adriana Adameova; Slavka Carnicka; Martina Nemcekova; Tara Kelly; Jana Matejikova; Eleftheria Galatou; Eleftheria Barlaka; Antigone Lazou
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  General physiology and biophysics     Volume:  30     ISSN:  0231-5882     ISO Abbreviation:  Gen. Physiol. Biophys.     Publication Date:  2011 Dec 
Date Detail:
Created Date:  2011-12-01     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8400604     Medline TA:  Gen Physiol Biophys     Country:  Slovakia    
Other Details:
Languages:  eng     Pagination:  329-41     Citation Subset:  IM    
Affiliation:
Institute for Heart Research, Slovak Academy of Sciences, Centre of Excellence NOREG SAS, Bratislava, Slovak Republic. usrdravi@savba.sk.
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