Targeting phosphatidylinositol 3-kinase-Akt through hepatocyte growth factor for cardioprotection

Rosalinda Madonna, Roberto Bolli, Gregg Rokosh, Raffaele De Caterina

Research output: Contribution to journalReview articlepeer-review

11 Scopus citations


Several growth factors have been shown to protect the cardiomyocyte from the detrimental effects of acute ischemia-reperfusion injury, through the activation of a variety of cell-surface receptors and the subsequent recruitment of a number of intracellular signal transduction pathways. Among these growth factors, hepatocyte growth factor (HGF), also named as scatter factor, acts by recruiting the phosphatidylinositol 3-kinase (PI3K)-Akt signal transduction pathway, linked to cardioprotection, at the time of myocardial infarction and myocardial reperfusion. HGF has been reported to increase in the early phase of myocardial infarction, and has been shown to have mitogenic, angiogenic, antiapoptotic and antifibrotic activities in cardiac myocytes and endothelial cells. Also, endogenous HGF may play an important role in the regeneration of endothelial cells and cardiomyocytes by promoting angiogenesis and inhibiting apoptosis during remodeling of the ischemic myocardium. Thus, HGF has the potential to emerge as a cardioprotective agent for the treatment of several pathological cardiac conditions. Here we review the role of HGF with respect to its ability to confer direct myocardial protection in the setting of ischemia-reperfusion injury, focusing on the main underlying signaling pathway involved.

Original languageEnglish
Pages (from-to)249-253
Number of pages5
JournalJournal of Cardiovascular Medicine
Issue number4
StatePublished - Apr 2013


  • Akt
  • Apoptosis
  • Cardioprotection
  • Hepatocyte growth factor
  • MET receptor
  • PI3K
  • Phosphatidylinositol 3-kinase


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