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- W2029305763 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." @default.
- W2029305763 created "2016-06-24" @default.
- W2029305763 creator A5007189559 @default.
- W2029305763 creator A5064803348 @default.
- W2029305763 date "2011-08-01" @default.
- W2029305763 modified "2023-10-15" @default.
- W2029305763 title "PPAR-γ and AMPK – Advantageous targets for myocardial ischemia/reperfusion therapy" @default.
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- W2029305763 doi "https://doi.org/10.1016/j.bcp.2011.04.004" @default.
- W2029305763 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21536015" @default.
- W2029305763 hasPublicationYear "2011" @default.
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