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Description
Guided by the BiBi kinetic mechanism of NNMT, bisubstrate inhibitors have been developed to simultaneously occupy both substrate and cofactor binding sites to mimic the transition state
Conversely, pharmacologic inhibition of GSK3 (using 1-azakenpaullone) increased supporting cell proliferation in a -catenin dependent manner, indicating that the effects are mediated by canonical Wnt signaling
In the context of DCM, chronic hyperglycemia disrupts fatty acid metabolism, leading to ACSL4 overexpression, increased PUFA-CoA production, and accelerated lipid peroxidation
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