SMAD3 and Sepsis: Sun et al. found that thrombospondin-1 (THBS1) and upstream stimulatory factor 2 (USF2) were highly expressed in patients with sepsis-induced AKI and that USF2 upregulated THBS1 expression to activate the TGF-β/Smad3/NLRP3/caspase-1 signalling pathway and stimulate pyroptosis, ultimately exacerbating sepsis-induced AKI [49].