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(121) published in 2024 revealed a novel mechanism by which AhR, as a uremic toxin receptor, promotes renal senescence and fibrosis: IS upregulates and activates AhR in renal tubular epithelial cells, and AhR can interact with peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), promoting its ubiquitin-mediated degradation through its E3 ubiquitin ligase activity, thereby inhibiting mitochondrial biogenesis
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