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Instead, it inhibits an enzyme called NNMT, which shifts cell metabolism toward fat oxidation and muscle preservation

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The binding of C-Met to HGF initiates the receptors innate kinase activity, followed by the formation of a multisubstrate docking site for the intracellular junction protein, which recruits signaling molecules due to homologous dimerization and autophosphorylation at Tyr1234 and Tyr1235 and subsequent phosphorylation at Tyr1349 and Tyr1356 at the c-terminal tail (Birchmeier et al., 2003

This dual insult exacerbates endothelial dysfunction and promotes pathological vascular remodeling and sclerosis, creating a vicious cycle that elevates blood pressure [198, 218]