Open AccessDeletion of podocyte STAT3 mitigates the entire spectrum of HIV-1-associated nephropathy
Author(s) -
Leyi Gu,
Yan Dai,
Jianing Xu,
Sandeep K. Mallipattu,
Lewis Kaufman,
Paul E. Klotman,
John Cijiang He,
Peter Y. Chuang
Publication year - 2013
Publication title -
aids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.195
H-Index - 216
eISSN - 1473-5571
pISSN - 0269-9370
DOI - 10.1097/qad.0b013e32835f1ea1
Subject(s) - podocyte , stat3 , cancer research , biology , stat protein , pathogenesis , nephropathy , glomerulosclerosis , diabetic nephropathy , albuminuria , microbiology and biotechnology , immunology , signal transduction , kidney , endocrinology , proteinuria , diabetes mellitus
HIV-1 gene expression in kidney epithelial cells is thought to be responsible for the pathogenesis of HIV-1-associated nephropathy (HIVAN). Signal transducer and activator of transcription (STAT) 3 signaling is activated in podocytes of patients with HIVAN and drives the dedifferentiation and proliferation of podocytes in culture. We confirm here that deletion of podocyte STAT3 is sufficient to mitigate the glomerular as well as tubulointerstitial findings of HIVAN.