This also disrupted the pro-fibrotic pathways of TGFβ/Smad and Wnt/β-catenin, altering pro-fibrotic protein levels in kidney cells treated with TGFβ and lessening renal fibrosis caused by one-sided ureteral blockage, suggesting SIN’s ability to suppress oxidative stress and safeguard the kidneys (110). Here, TGFB1 is linked to renal fibrosis.