title: Angiotensin II-mediated Nrf2 down-regulation: a potential causing factor for renal fibrosis?
abstract: Epithelial-mesenchymal transition (EMT), a phenotype conversion of epithelial cells to myofibroblasts, is closely related with pathogenesis of renal fibrosis. Although it has been known that angiotensin II (ATII) stimulates EMT process in various cell types, the precise molecular mechanisms had not been clearly demonstrated. In this issue, Kang et al. show that AII suppresses NF-E2-related factor 2 (Nrf2) signaling and enhances transforming growth factor-β1's activity to induce EMT in renal epithelial cells (Kang et al., 2011). They suggest that ATII-mediated EMT stimulating effect may result from the increased oxidative stress via defect in Nrf2-antioxidant system. This report proposes a possible mechanism of ATII-mediated renal fibrosis.
authors.affiliation: BK21 Project Team, College of Pharmacy, Chosun University, Gwangju 501-759, Republic of Korea. kwkang@chosun.ac.kr
authors.forename: Keon Wook
authors.initials: KW
authors.lastname: Kang
mesh_terms: D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D004847:Epithelial Cells / Q000378:metabolism*; D005786:Gene Expression Regulation; D007668:Kidney / Q000378:metabolism*; D051267:NF-E2-Related Factor 2 / Q000037:antagonists & inhibitors*; D015398:Signal Transduction
chemical_list: D051267:NF-E2-Related Factor 2; C495636:Nfe2l2 protein, mouse; D000804:Angiotensin II