ArticleDisease models & mechanisms2025
Notch3 deletion regulates HIV-1 gene expression and systemic inflammation to ameliorate chronic kidney disease.
Article in Disease models & mechanisms, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Preterm Birth Increases Susceptibility to Hyperglycemia-Induced Kidney Injury With Sex-Specific Differences in Structural and Molecular Responses.Endocrinology, diabetes & metabolism · 2026Article
Corrections and comments
- Update of
Authors and funding
20 authors.
Funding
Abstract
Anti-retroviral therapy (ART) has decreased human immunodeficiency virus (HIV)-1-associated morbidity. However, despite ART, immune cells remain latently infected, leading to chronic inflammation and HIV-1-associated comorbidities. New strategies are needed to target viral proteins and inflammation. We found activation of Notch3 in renal cells of the HIV-1 transgenic mouse model (HIV-Tg26) and in patients with HIV-associated nephropathy. We hypothesized that targeting NOTCH3 activation constitutes an effective therapy for HIV-related chronic kidney disease. We generated HIV-Tg26 mice with Notch3 knocked out (Tg-N3KO). Compared to HIV-Tg26 mice at 3 months, Tg-N3KO mice showed a marked reduction in renal injury, skin lesions and mortality rate. They also showed reduced renal infiltrating cells and significantly reduced expression of HIV genes. Moreover, Notch3 activated the HIV long terminal repeat promoter, and induction of HIV-1 increased Notch3 activation, indicating a feedback mechanism. Further, bone marrow-derived macrophages from HIV-Tg26 mice showed activation of Notch3, indicating systemic effects. Consistent with that observation, systemic levels of TNF and MCP-1 were reduced in Tg-N3KO compared to HIV-Tg26 mice. Thus, Notch3 deletion/inhibition has a dual-therapeutic effect in HIV-related chronic kidney disease, which might extend to other HIV-related pathologies.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.