ArticleKidney international2009
Accelerated development of collapsing glomerulopathy in mice congenic for the HIVAN1 locus.
Article in Kidney international, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 31 citations in OpenAlex.
- 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
- GWAS in Mice Maps Susceptibility to HIV-Associated Nephropathy to theJournal of the American Society of Nephrology : JASN · 2022Article
- Kidney Disease in HIV: Moving beyond HIV-Associated Nephropathy.Journal of the American Society of Nephrology : JASN · 2017Review
- Refinement of the HIVAN1 Susceptibility Locus on Chr. 3A1-A3 via Generation of Sub-Congenic Strains.PloS one · 2016Article
- Apolipoprotein L1 (APOL1) Variants (Vs) a possible link between Heroin-associated Nephropathy (HAN) and HIV-associated Nephropathy (HIVAN).Frontiers in microbiology · 2015Review
- Modulation of renin angiotensin system predominantly alters sclerotic phenotype of glomeruli in HIVAN.Histology and histopathology · 2014Article
- HIV associated lupus like nephropathy.Ethiopian journal of health sciences · 2014Article
- mTOR plays a critical role in p53-induced oxidative kidney cell injury in HIVAN.American journal of physiology. Renal physiology · 2013Article
- APOL1 variants increase risk for FSGS and HIVAN but not IgA nephropathy.Journal of the American Society of Nephrology : JASN · 2011Article
- Identification of the nephropathy-susceptibility locus HIVAN4.Journal of the American Society of Nephrology : JASN · 2011Article
- Advances in our understanding of the pathogenesis of HIV-1 associated nephropathy in children.Future virology · 2011Article
- HIV-associated nephropathy: pathogenesis.Current opinion in nephrology and hypertension · 2011Review
- The molecular pathogenesis of HIV-1 associated nephropathy: recent advances.Journal of molecular medicine (Berlin, Germany) · 2011Review
- Recent developments in HIV-related kidney disease.HIV therapy · 2010Article
- HIV-associated nephropathy: role of mammalian target of rapamycin pathway.The American journal of pathology · 2010Article
- Genetics of focal segmental glomerulosclerosis and human immunodeficiency virus-associated collapsing glomerulopathy: the role of MYH9 genetic variation.Seminars in nephrology · 2010Review
- Susceptibility loci for murine HIV-associated nephropathy encode trans-regulators of podocyte gene expression.The Journal of clinical investigation · 2009Article
- Genetic susceptibility to HIV-associated nephropathy.The Journal of clinical investigation · 2009Article
- Collapsing glomerulopathy: beyond serendipity in mouse genetics.Kidney international · 2009Article
- Myeloma Cast Nephropathy an Unusual Association with HIV Infection Presenting with Renal Dysfunction.Indian journal of nephrologyArticle
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9 authors at 3 institutions in 1 country.
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Abstract
HIV-1 transgenic mice on the FVB/NJ background (TgFVB) are a well validated model of HIV-associated nephropathy (HIVAN). A mapping study between TgFVB and CAST/EiJ (CAST) strains showed this trait to be influenced by a major susceptibility locus on chromosome 3A1-A3 (HIVAN1), with CAST alleles associated with increased risk of disease. We introgressed a 50 Mb interval, encompassing this HIVAN1 locus, from CAST into the TgFVB genome (TgFVB-HIVAN1(CAST) congenic mice). Compared to the TgFVB strain, these congenic mice developed an earlier onset of proteinuria, a rapid progression to kidney failure, and increased mortality. A prospective study of these congenic mice also showed that they had a significantly greater histologic and biochemical evidence of glomerulopathy with one-third of mice developing global glomerulosclerosis by 6 weeks of age. An F2 cross between TgFVB and the congenic mice identified a significant linkage (LOD=3.7) to a 10 cM interval within the HIVAN1 region between D3Mit167 and D3Mit67 resulting in a 60% reduction of the original interval. These data independently confirm that a gene on chromosome 3A1-A3 increases susceptibility to HIVAN, resulting in early onset and rapid progression of kidney disease. These mice represent a new model to study the development and progression of collapsing glomerulopathy.
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