act(a(HBP:"advanced glycation end product")) increases p(HGNC:MAPT, pmod(HBP:hyperphosphorylation))

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PubMed:25987199

In this study, we demonstrated that GLP-1RA could inhibit oxidative stress and repair mitochondrial damage in addition to decreasing tau hyperphosphorylation in PC12 cells treated with AGEs. Importantly, we first observed AGEs in the circulatory system could induce tau hyperphosphorylation after we injected AGEs (1μg/kg bodyweight) into the mice tail vein. We found GLP-1RA could promote mitochondrial biogenesis and antioxidant system via regulating peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) signaling pathway in vivo besides down-regulating the activity of glycogen synthase kinase 3β (GSK-3β) to reverse tau hyperphosphorylation directly.

Related Edges 9

• act(a(GO:mitochondrion)) positiveCorrelation act(p(MGI:Ppargc1a))
• act(a(HBP:"advanced glycation end product")) negativeCorrelation act(p(MGI:Glp1r))
• act(p(HGNC:GLP1R)) decreases bp(MESH:"Oxidative Stress")
• act(p(HGNC:GLP1R)) increases act(a(GO:mitochondrion))
• act(p(MGI:Glp1r)) increases act(p(MGI:Ppargc1a))
• act(p(MGI:Glp1r)) decreases act(p(MGI:Gsk3b), ma(kin))
• act(p(MGI:Glp1r)) decreases p(MGI:Mapt, pmod(HBP:hyperphosphorylation))
• act(p(MGI:Glp1r)) negativeCorrelation act(a(HBP:"advanced glycation end product"))
• act(p(MGI:Ppargc1a)) positiveCorrelation act(a(GO:mitochondrion))

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