TGF-β1 treatment inhibited the expression of PAs and induced the production of their inhibitor PAI-1, leading to the reduced degradation of ECM.352 Tissue inhibitor of metalloproteinase that was an inhibitor of MMP was upregulated by TGF-β/Smad signaling in CKD and promoted age-related renal fibrosis.353 Precursors like TECs, endothelial cells, and macrophages convert into myofibroblasts through partial epithelial-mesenchymal transition (partial EMT), endothelial-mesenchymal transition (EndMT), and MMT, respectively. This evidence concerns the gene TGFB1 and chronic kidney disease.