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The key pathways including lipotoxicity and oxidative stress (involving NLRP3 inflammasome, MAPK, PI3K/Akt, and RAAS signaling), inflammation (via NF-B, NLRP3 inflammasome, JAK-STAT, Toll-like receptor, and cGAS-STING pathways), and fibrosis/ECM production (driven by TGF-, Wnt, RAAS, and Notch signaling) have been identified and reported in CKD progression [235]

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When blood glucose levels return to normal, the incretin effect diminishes, maintaining blood glucose at normal levels with high safety (60, 61)

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