title: PPAR-γ and AMPK--advantageous targets for myocardial ischemia/reperfusion therapy.
abstract: 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.affiliation: Department of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, University at Buffalo-SUNY, 3435 Main Street, Buffalo, NY 14214, United States.
authors.forename: Alex
authors.initials: A
authors.lastname: Morrison
authors.forename: Ji
authors.initials: J
authors.lastname: Li
mesh_terms: D000263:Adenylate Kinase / Q000235:genetics / Q000378:metabolism*; D002317:Cardiovascular Agents / Q000627:therapeutic use*; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology* / Q000517:prevention & control*; D047495:PPAR gamma / Q000378:metabolism*
chemical_list: D002317:Cardiovascular Agents; D047495:PPAR gamma; D000263:Adenylate Kinase