ArticleAmerican journal of physiology. Renal physiology2013
Inhibition of Notch pathway attenuates the progression of human immunodeficiency virus-associated nephropathy.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Cell cycle disorders in podocytes: an emerging and increasingly recognized phenomenon.Cell death discovery · 2025Review
- Notch3 deletion regulates HIV-1 gene expression and systemic inflammation to ameliorate chronic kidney disease.Disease models & mechanisms · 2025Article
- PKR activation-induced mitochondrial dysfunction in HIV-transgenic mice with nephropathy.eLife · 2024Article
- Notch3 deletion regulates HIV-1 gene expression and systemic inflammation to ameliorate chronic kidney disease.bioRxiv : the preprint server for biology · 2024Article
- Liraglutide Ameliorates Renal Endothelial Dysfunction in Diabetic Rats Through the Inhibition of the Dll4/Notch2 Pathway.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- HIV-1 subtype B Tat enhances NOTCH3 signaling in astrocytes to mediate oxidative stress, inflammatory response, and neuronal apoptosis.Journal of neurovirology · 2023Article
- Quinomycin A reduces cyst progression in polycystic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Ciclopirox olamine induces ferritinophagy and reduces cyst burden in polycystic kidney disease.JCI insight · 2021Article
- Hantavirus Induced Kidney Disease.Frontiers in medicine · 2021Review
- Notch4 activation aggravates NF-κB-mediated inflammation in HIV-1-associated nephropathy.Disease models & mechanisms · 2019Article
- γ-secretase inhibitor DAPT mitigates cisplatin-induced acute kidney injury by suppressing Notch1 signaling.Journal of cellular and molecular medicine · 2019Article
- Podocyte-Specific Induction of Krüppel-Like Factor 15 Restores Differentiation Markers and Attenuates Kidney Injury in Proteinuric Kidney Disease.Journal of the American Society of Nephrology : JASN · 2018Article
- Aberrant activation of Notch-1 signaling inhibits podocyte restoration after islet transplantation in a rat model of diabetic nephropathy.Cell death & disease · 2018Article
- Aberrant Regulation of Notch3 Signaling Pathway in Polycystic Kidney Disease.Scientific reports · 2018Article
- Molecular Mechanisms of Injury in HIV-Associated Nephropathy.Frontiers in medicine · 2018Review
- Transcriptome-based network analysis reveals renal cell type-specific dysregulation of hypoxia-associated transcripts.Scientific reports · 2017Article
- The role of Notch signaling in kidney podocytes.Clinical and experimental nephrology · 2017Review
- HIV-associated nephropathies: epidemiology, pathology, mechanisms and treatment.Nature reviews. Nephrology · 2015Review
- Kick it up a notch: Notch signaling and kidney fibrosis.Kidney international supplements · 2014Review
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Authors and funding
9 authors at 5 institutions in 1 country.
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Abstract
The Notch pathway is an evolutionarily conserved signaling cascade that is critical in kidney development and has also been shown to play a pathogenetic role in a variety of kidney diseases. We have previously shown that the Notch signaling pathway is activated in human immunodeficiency virus-associated nephropathy (HIVAN) as well as in a rat model of the disease. In this study, we examined Notch signaling in the well established Tg26 mouse model of HIVAN. Notch signaling components were distinctly upregulated in the kidneys of these mice as well as in immortalized podocytes derived from these mice. Notch1 and Notch4 were upregulated in the Tg26 glomeruli, and Notch4 was also expressed in tubules. Notch ligands Jagged1, Jagged2, Delta-like1, and Delta-like 4 were all upregulated in the tubules of Tg26 mice, but glomeruli showed minimal expression of Notch ligands. To examine a potential pathogenetic role for Notch in HIVAN, Tg26 mice were treated with GSIXX, a gamma secretase inhibitor that blocks Notch signaling. Strikingly, GSIXX treatment resulted in significant improvement in both histological kidney injury scores and renal function. GSIXX-treated Tg26 mice also showed diminished podocyte proliferation and dedifferentiation, cellular hallmarks of the disease. Moreover, GSIXX blocked podocyte proliferation in vitro induced by HIV proteins Nef and Tat. These studies suggest that Notch signaling can promote HIVAN progression and that Notch inhibition may be a viable treatment strategy for HIVAN.
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