Additional studies have reported that macrophage-derived sEV containing angiotensin II type 1 receptor played an important role in BLM-induced pulmonary fibrosis (25), and macrophage-derived sEV also activated the fibroblast in an endoplasmic reticulum stress-dependent manner to mediate silica-induced pulmonary fibrosis (26). This evidence concerns the gene AGTR1 and pulmonary fibrosis.