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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 (PGC1), promoting its ubiquitin-mediated degradation through its E3 ubiquitin ligase activity, thereby inhibiting mitochondrial biogenesis

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If this is the scenario, then turning to stem cell therapy might be the better choice

Hansson GK, Massachusetts Medical Society (2005) Inflammation, atherosclerosis, and coronary artery disease

Consider platelet function testing (e.g., TEG with platelet mapping) for patients on antiplatelet medications undergoing a procedure