HGF/c-Met signaling is a well-established oncogenic pathway: c-Met is amplified or overexpressed in multiple cancers (gastric, lung, renal, hepatocellular) HGF/c-Met activation promotes tumor cell proliferation, survival, invasion, and metastasis c-Met inhibitors are FDA-approved cancer drugs (cabozantinib, crizotinib, capmatinib) A compound that potentiates HGF/c-Met signaling raises theoretical concerns about promoting tumor growth or transformation with chronic use
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Loss of GSH homeostasis as occurs in ageing, chronic inflammation, and metabolic disease shifts S-glutathionylation patterns and dysregulates the signalling networks that depend on them
In mice, group A viruses are tropic for striated muscle, whereas CVB strains have tropism for the pancreas, heart, liver, brown fat, central nervous system, and striated muscle (136)