ReviewJournal of molecular medicine (Berlin, Germany)2011
The molecular pathogenesis of HIV-1 associated nephropathy: recent advances.
Review in Journal of molecular medicine (Berlin, Germany), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Notch3 deletion regulates HIV-1 gene expression and systemic inflammation to ameliorate chronic kidney disease.Disease models & mechanisms · 2025Article
- Notch3 deletion regulates HIV-1 gene expression and systemic inflammation to ameliorate chronic kidney disease.bioRxiv : the preprint server for biology · 2024Article
- Notch4 activation aggravates NF-κB-mediated inflammation in HIV-1-associated nephropathy.Disease models & mechanisms · 2019Article
- Hyperglycemia enhances kidney cell injury in HIVAN through down-regulation of vitamin D receptors.Cellular signalling · 2015Article
- Review
- Inhibition of Notch pathway attenuates the progression of human immunodeficiency virus-associated nephropathy.American journal of physiology. Renal physiology · 2013Article
- Nef interaction with actin compromises human podocyte actin cytoskeletal integrity.Experimental and molecular pathology · 2013Article
- Renal dysfunction in the setting of HIV/AIDS.Current HIV/AIDS reports · 2012Review
- Sirolimus modulates HIVAN phenotype through inhibition of epithelial mesenchymal transition.Experimental and molecular pathology · 2012Article
- Human apolipoprotein L1 (ApoL1) in cancer and chronic kidney disease.FEBS letters · 2012Review
- APOL1 risk variants predict histopathology and progression to ESRD in HIV-related kidney disease.Journal of the American Society of Nephrology : JASN · 2012Article
- APOL1 variants increase risk for FSGS and HIVAN but not IgA nephropathy.Journal of the American Society of Nephrology : JASN · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HIV-1-associated nephropathy (HIVAN) is a major complication of HIV-1 infection, frequently resulting in kidney failure. HIVAN arises due to HIV-1-induced dysregulation of podocytes, the glomerular epithelial cells that establish and maintain the kidney filtration barrier. Host genetic factors are important for the development of HIVAN. The risk of HIVAN is greatest in populations of African ancestry, and is attributable to a genetic variation at the APOL1 locus on chromosome 22. Mouse models of HIVAN enable delineation of dysregulated pathways underlying disease. Identification of HIVAN susceptibility loci in a mouse model, combined with expression quantitative trait locus mapping, has demonstrated that murine HIVAN loci transregulate podocyte gene expression. HIV-1 induces perturbations in podocyte expression response, suggesting that HIV-1 potentially interferes with compensatory pathways that normally restore cellular homeostasis in the face of genetic mutations. These findings present a framework for identification of podocyte transregulators and reconstruction of the molecular networks connecting susceptibility genes to the development of nephropathy.
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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 OpenQuestion graph.