Angiotensin II Activation of mTOR Results in Tubulointerstitial Fibrosis through Loss of N-Cadherin | Zendy

Adam WhaleyConnell | Zendy; Javad Habibi | Zendy; Zachary Panfili | Zendy; Melvin R. Hayden | Zendy; Sarika Bagree | Zendy; Ravi Nistala | Zendy; Safwan Hyder | Zendy; Bennett Krueger | Zendy; Vincent G. DeMarco | Zendy; Lakshmi Pulakat | Zendy; Carlos M. Ferrario | Zendy; Alan Parrish | Zendy; James R. Sowers | Zendy

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Angiotensin 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 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.

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