ag-490 and Fibrosis

ag-490 has been researched along with Fibrosis* in 2 studies

Other Studies

2 other study(ies) available for ag-490 and Fibrosis

ArticleYear
MUC1 Promotes Mesangial Cell Proliferation and Kidney Fibrosis in Diabetic Nephropathy Through Activating STAT and β-Catenin Signal Pathway.
    DNA and cell biology, 2021, Volume: 40, Issue:10

    Topics: Animals; beta Catenin; Cell Proliferation; Cells, Cultured; Diabetic Nephropathies; Fibronectins; Fibrosis; Kidney; Male; Mesangial Cells; Mice; Mice, Inbred C57BL; Mucin-1; Signal Transduction; STAT Transcription Factors; Sulfonamides; Tyrphostins

2021
Tyrphostin AG490 reduces inflammation and fibrosis in neonatal obstructive nephropathy.
    PloS one, 2019, Volume: 14, Issue:12

    Congenital obstructive nephropathy is the main cause of end-stage renal disease in infants and children. Renal insufficiency is due to impaired growth and maturation in the developing kidney with obstruction. Congenital obstructive nephropathy leads to cytokine mediated inflammation and the development of interstitial fibrosis. The Janus kinase-2 (JAK-2) and Signal Transducer and Activator of Transcription'-3 (STAT3) are involved in cytokine production, inflammation, and interstitial fibrosis.. We studied the role of JAK2/STAT3 in a model of congenital obstructive nephropathy using unilateral ureteral obstruction (UUO) in neonatal mice at the second day of life. Cytokine production, inflammation, and interstitial fibrosis were analyzed in obstructed and sham operated kidneys of neonatal mice treated with or without JAK2/STAT3 inhibitor Tyrphostin AG490. To mimic obstruction and distension, proximal tubular cells were stretched in vitro.. We show that STAT3 is highly activated in the developing kidney with obstruction and in proximal tubular cells following stretch. JAK2/STAT3 activation mediates cytokine release and leukocyte recruitment into neonatal kidneys after UUO. Pharmacological blockade of JAK2/STAT3 by Tyrphostin AG490 reduced inflammation, tubular apoptosis, and interstitial fibrosis. JAK2/STAT3 blockade decreased pro-inflammatory and profibrotic mediators in tubular cells.. Our findings provide evidence that JAK2/STAT3 mediates inflammation and fibrosis in the developing kidney with obstruction. Blocking JAK2/STAT3 may prove beneficial in congenital obstructive nephropathy in children.

    Topics: Animals; Animals, Newborn; Enzyme Inhibitors; Fibrosis; Inflammation; Janus Kinase 2; Mice; STAT3 Transcription Factor; Tyrphostins; Ureteral Obstruction

2019