LRG1 and glomerulosclerosis: (108) reported that Lrg1 protein derived from GECs may translocate to the mesangial region, exacerbating glomerulosclerosis through upregulation of TGF-β signaling and increasing fibrosis by upregulating Plasminogen activator inhibitor-1 (PAI-1) gene expression (a pro-fibrotic marker) via the p38 pathway in mesangial cells.