Open AccessInhibition of cellular transdifferentiation by losartan minimizes but does not reverse type 2 diabetes-induced renal fibrosis
Author(s) -
Carine Prisco Ari,
Edgar Maquigussa,
Clévia Santos Passos,
Luciana G. Pereira,
Mirian Aparecida Boim
Publication year - 2014
Publication title -
jraas. journal of the renin-angiotensin-aldosterone system/journal of the renin-angiotensin-aldosterone system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.457
H-Index - 46
eISSN - 1752-8976
pISSN - 1470-3203
DOI - 10.1177/1470320313497817
Subject(s) - losartan , transdifferentiation , fibrosis , endocrinology , medicine , angiotensin ii , valsartan , angiotensin ii receptor type 1 , diabetic nephropathy , type 2 diabetes , diabetes mellitus , receptor , biology , microbiology and biotechnology , stem cell , blood pressure
Transformer Growth Factor (TGF-β1) and angiotensin II (AngII) induce epithelial mesenchymal transition (EMT) and myofibroblastic transdifferentiation (MFT) contributing to renal fibrosis. The present study evaluated the capacity of an AT1 receptor blocker (losartan) to induce the regression of pre-existing fibrosis via interference with MFT and EMT in a rat model of type 2 diabetes, and in cultured mesangial cells (MCs) stimulated with high glucose and AngII.