TNFRSF1A and fibrosis: Their renoprotective effects stem from coordinated suppression of inflammatory cascades like TNFR1/IL-6/MMP7 downregulation, oxidative stress via AGE-RAGE-ROS axis interruption, and metabolic reprogramming through PKM2-mediated glycolytic flux reduction, collectively attenuating EMT and tubulointerstitial fibrosis [135,136,137].