In renal endothelial cells, TGF-β1 mediates renal fibrosis by inducing modifications characteristic of endothelial–mesenchymal transition (EndMT) [39,40], a phenomenon whereby endothelial cells begin to express the characteristics of mesenchymal cells, with the acquisition of mesenchymal markers like α-smooth muscle actin (αSMA) [9] and loss of endothelial markers like VE-cadherin and CD31 [9,40]. Here, TGFB1 is linked to renal fibrosis.