HGF/Met tyrosine kinase receptor in heart physiology and pathophysiology

Our work has mainly investigated the role of HGF/Met tyrosine kinase receptor signaling in the heart during physiological and pathological conditions. Targeting HGF/Met activation in neonatal heart in vivo modulates the gene expression program involved in cardiomyogenesis. Furthermore, sustained activation of Met pathways in postnatal cardiomyocytes in vivo strongly increases the heart growth. Our research has also extended to the influence of Met activation in the heart protection against injury. Importantly, we have shown that Met stimulation by HGF protects cardiac cells from hypoxic damage both in vivo, in a mouse model of myocardial infarction, and in vitro, in cardiomyoblast cells cultured in low oxygen tension. Recently, we have shown that HGF protects cardiac cells from antracyclinemediated cardiotoxicity, showing that the induction of ROS-triggered apoptosis and autophagy is attenuated by HGF. In addition, our approach get closer to the clinic, with the development of original tools for therapeutic application.