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Similarly, in mesangial cells, GLP-1 receptor agonists have been shown to suppress either high-glucose-induced or AGEs-induced pro-fibrotic signalling pathways, including NF-B activation and TGF-1 expression, leading to reduced ECM deposition [60,61], and to suppress their proliferation via AMPK activation [62]

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In vitro, rat PSCs were treated with low glucose, high glucose, or high glucose plus glutathione to explore the mechanism of high glucose-induced PSC activation and the downstream effects of glutathione

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