ArticleJournal of the American Society of Nephrology : JASN2008
Maternal environment interacts with modifier genes to influence progression of nephrotic syndrome.
Article in Journal of the American Society of Nephrology : JASN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Rare heterozygous variants in paediatric steroid resistant nephrotic syndrome - a population-based analysis of their significance.Scientific reports · 2024Article
- Review
- Evolution, kidney development, and chronic kidney disease.Seminars in cell & developmental biology · 2019Review
- A transcriptional network underlies susceptibility to kidney disease progression.EMBO molecular medicine · 2012Article
- Identification of the nephropathy-susceptibility locus HIVAN4.Journal of the American Society of Nephrology : JASN · 2011Article
- TGF-alpha mediates genetic susceptibility to chronic kidney disease.Journal of the American Society of Nephrology : JASN · 2011Article
- Podocin inactivation in mature kidneys causes focal segmental glomerulosclerosis and nephrotic syndrome.Journal of the American Society of Nephrology : JASN · 2009Article
- 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
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Authors and funding
15 authors at 5 institutions in 5 countries.
Funding
Abstract
Mutations in the NPHS2 gene, which encodes podocin, are responsible for some cases of sporadic and familial autosomal recessive steroid-resistant nephrotic syndrome. Inter- and intrafamilial variability in the progression of renal disease among patients bearing NPHS2 mutations suggests a potential role for modifier genes. Using a mouse model in which the podocin gene is constitutively inactivated, we sought to identify genetic determinants of the development and progression of renal disease as a result of the nephrotic syndrome. We report that the evolution of renal disease as a result of nephrotic syndrome in Nphs2-null mice depends on genetic background. Furthermore, the maternal environment significantly interacts with genetic determinants to modify survival and progression of renal disease. Quantitative trait locus mapping suggested that these genetic determinants may be encoded for by genes on the distal end of chromosome 3, which are linked to proteinuria, and on the distal end of chromosome 7, which are linked to a composite trait of urea, creatinine, and potassium. These loci demonstrate epistatic interactions with other chromosomal regions, highlighting the complex genetics of renal disease progression. In summary, constitutive inactivation of podocin models the complex interactions between maternal and genetically determined factors on the progression of renal disease as a result of nephrotic syndrome in mice.
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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.