Open AccessAngiotensin II Activation of mTOR Results in Tubulointerstitial Fibrosis through Loss of N-Cadherin
Author(s) -
Adam WhaleyConnell,
Javad Habibi,
Zachary Panfili,
Melvin R. Hayden,
Sarika Bagree,
Ravi Nistala,
Safwan Hyder,
Bennett Krueger,
Vincent G. DeMarco,
Lakshmi Pulakat,
Carlos M. Ferrario,
Alan R. Parrish,
James R. Sowers
Publication year - 2011
Publication title -
american journal of nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.394
H-Index - 85
eISSN - 1421-9670
pISSN - 0250-8095
DOI - 10.1159/000329327
Subject(s) - endocrinology , medicine , angiotensin ii , fibrosis , glomerulosclerosis , kidney , receptor , proteinuria
Angiotensin (Ang) II contributes to tubulointerstitial fibrosis. Recent data highlight mammalian target of rapamycin (mTOR)/S6 kinase 1 (S6K1) signaling in tubulointerstitial fibrosis; however, the mechanisms remain unclear. Thereby, we investigated the role of Ang II on mTOR/S6K1-dependent proximal tubule (PT) injury, remodeling, and fibrosis.