Although numerous strategies have been developed to reduce the initial ischemic insult and cellular injury that occurs during myocardial infarction (MI), few have progressed into the clinical arena. The epidemiologic and economic impact of MI necessitates the development of innovative therapies to rapidly and effectively reduce the initial injury and subsequent cardiac dysfunction. The Eph receptors and their cognate ligands, the ephrins, are the largest family of receptor tyrosine kinases, and their signaling has been shown to play a diverse role in various cellular processes. The recent advances in the study of ephrin-Eph signaling have shown promising progress in many fields of medicine. They have been implicated in the pathophysiology of various cancers and in the regulation of inflammation and apoptosis. Recent studies have shown that manipulation of ephrin-Eph cell signaling can favorably influence cardiomyocyte viability and ultimately preserve cardiac function post-MI. In this article, we explore the hypothesis that manipulation of ephrin-Eph signaling may potentially be a novel therapeutic target in the treatment of MI through alteration of the cellular processes that govern injury and wound healing.
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