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Description
In those preclinical models it has been reported to promote angiogenesis the growth of new blood vessels through the VEGFR2AkteNOS / nitric-oxide pathway, which may help explain its observed effects on healing [1] [4]
38,5658 However, instead of enhancing the injury mechanism as intended, this modulation changed the injury process altogether from a protein adduct-driven signaling process to one dominated by LPO
2008;138(10):2045S9S
Concurrent disruption of the AMPKNrf2 axis further weakens antioxidant capacity and exacerbates mitochondrial dysfunction
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It is involved in regulating gametogenesis, embryonic and placental growth, as well as imprinting and epigenesis
