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This review summarizes the dysbiosis of gut microbiota in kidney disease and elucidates the underlying molecular mechanisms of microbial dysbiosis through a broad spectrum of signaling pathways, such as TGF-/Smad, IB/NF-B, Keap1/Nrf2, phosphatidylinositol-3 kinase (PI3K), and mitogen-activated protein kinases (MAPK), as well as key mediators, such as AHR, NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, and G protein-coupled receptor 43 (GPR43), via alteration of diverse metabolites

Because most existing POAG polygenic risk scores have been derived largely from European-ancestry cohorts, their transferability to other populations remains limited

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