| First Author | Feng W | Year | 2021 |
| Journal | Am J Physiol Renal Physiol | Volume | 320 |
| Issue | 1 | Pages | F87-F96 |
| PubMed ID | 33283645 | Mgi Jnum | J:309591 |
| Mgi Id | MGI:6751773 | Doi | 10.1152/ajprenal.00401.2020 |
| Citation | Feng W, et al. (2021) Renoprotective effect of Stat1 deletion in murine aristolochic acid nephropathy. Am J Physiol Renal Physiol 320(1):F87-F96 |
| abstractText | Injured tubule epithelium stimulates a profibrotic milieu that accelerates loss of function in chronic kidney disease (CKD). This study tested the role of signal transducer and activator of transcription 1 (STAT1) in the progressive loss of kidney function in aristolochic acid (AA) nephropathy, a model of CKD. Mean serum creatinine concentration increased in wild-type (WT) littermates treated with AA, whereas Stat1(-/-) mice were protected. Focal increases in the apical expression of kidney injury molecule (KIM)-1 were observed in the proximal tubules of WT mice with AA treatment but were absent in Stat1(-/-) mice in the treatment group as well as in both control groups. A composite injury score, an indicator of proximal tubule injury, was reduced in Stat1(-/-) mice treated with AA. Increased expression of integrin-beta6 and phosphorylated Smad2/3 in proximal tubules as well as interstitial collagen and fibronectin were observed in WT mice following AA treatment but were all decreased in AA-treated Stat1(-/-) mice. The data indicated that STAT1 activation facilitated the development of progressive kidney injury and interstitial fibrosis in AA nephropathy. |
