ArticleThe Journal of clinical investigation2009
Susceptibility loci for murine HIV-associated nephropathy encode trans-regulators of podocyte gene expression.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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43 citing papers in PubMed, 70 citations in OpenAlex.
- Impact of Apolipoprotein L1-Associated Pregnancy Complications on Kidney Disease Phenotypes in a HIV-Associated Nephropathy Mouse Model.Kidney360 · 2026Article
- Mouse and human studies support DSTYK loss of function as a low-penetrance and variable expressivity risk factor for congenital urinary tract anomalies.Genetics in medicine : official journal of the American College of Medical Genetics · 2023Article
- HIV at 40: kidney disease in HIV treatment, prevention, and cure.Kidney international · 2022Review
- GWAS in Mice Maps Susceptibility to HIV-Associated Nephropathy to theJournal of the American Society of Nephrology : JASN · 2022Article
- Dysregulated Dynein-Mediated Trafficking of Nephrin Causes INF2-related Podocytopathy.Journal of the American Society of Nephrology : JASN · 2021Article
- Kidney Disease in HIV: Moving beyond HIV-Associated Nephropathy.Journal of the American Society of Nephrology : JASN · 2017Review
- Mouse chromosome 2 harbors genetic determinants of resistance to podocyte injury and renal tubulointerstitial fibrosis.BMC genetics · 2016Article
- Refinement of the HIVAN1 Susceptibility Locus on Chr. 3A1-A3 via Generation of Sub-Congenic Strains.PloS one · 2016Article
- APOL1 Genotype and Glomerular and Tubular Kidney Injury in Women With HIV.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2015Observational
- The association between APOL1 risk alleles and longitudinal kidney function differs by HIV viral suppression status.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2015Article
- Article
- Podocyte injury caused by indoxyl sulfate, a uremic toxin and aryl-hydrocarbon receptor ligand.PloS one · 2014Article
- Quantitative trait Loci for resistance to the congenital nephropathy in tensin 2-deficient mice.PloS one · 2014Article
- Host APOL1 genotype is independently associated with proteinuria in HIV infection.Kidney international · 2013Article
- Comparison of risk factors and outcomes in HIV immune complex kidney disease and HIV-associated nephropathy.Clinical journal of the American Society of Nephrology : CJASN · 2013Article
- Article
- HIV-associated nephropathy patients with and without apolipoprotein L1 gene variants have similar clinical and pathological characteristics.Kidney international · 2012Article
- A transcriptional network underlies susceptibility to kidney disease progression.EMBO molecular medicine · 2012Article
- Sirolimus modulates HIVAN phenotype through inhibition of epithelial mesenchymal transition.Experimental and molecular pathology · 2012Article
- Glomerular MYH9 expression is reduced by HIV-1.AIDS (London, England) · 2012Article
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14 authors at 4 institutions in 1 country.
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Abstract
Multiple studies have linked podocyte gene variants to diverse sporadic nephropathies, including HIV-1-associated nephropathy (HIVAN). We previously used linkage analysis to identify a major HIVAN susceptibility locus in mouse, HIVAN1. We performed expression quantitative trait locus (eQTL) analysis of podocyte genes in HIV-1 transgenic mice to gain further insight into genetic susceptibility to HIVAN. In 2 independent crosses, we found that transcript levels of the podocyte gene nephrosis 2 homolog (Nphs2), were heritable and controlled by an ancestral cis-eQTL that conferred a 3-fold variation in expression and produced reactive changes in other podocyte genes. In addition, Nphs2 expression was controlled by 2 trans-eQTLs that localized to the nephropathy susceptibility intervals HIVAN1 and HIVAN2. Transregulation of podocyte genes was observed in the absence of HIV-1 or glomerulosclerosis, indicating that nephropathy susceptibility alleles induce latent perturbations in the podocyte expression network. Presence of the HIV-1 transgene interfered with transregulation, demonstrating effects of gene-environment interactions on disease. These data demonstrate that transcript levels of Nphs2 and related podocyte-expressed genes are networked and suggest that the genetic lesions introduced by HIVAN susceptibility alleles perturb this regulatory pathway and transcriptional responses to HIV-1, increasing susceptibility to nephropathy.
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