Fibrosis-induced microvascular obliteration and vasoconstriction is mediated by vasoactive factors (e.g. angiotensin II and endothelin-1), which produce ischemia, glomerular hemodynamic alterations and further angiotensin II production, all of which amplify fibrogenesis and perpetuate damage [83,84] with the concourse of TGF-β1 and PDGF [85,86]. Here, AGT is linked to fibrosis.