ArticlePhysiological genomics2013
SORCS1 contributes to the development of renal disease in rats and humans.
Article in Physiological genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- The adducin saga: pleiotropic genomic targets for precision medicine in human hypertension-vascular, renal, and cognitive diseases.Physiological genomics · 2022Review
- Knockout ofThe Journal of pharmacology and experimental therapeutics · 2021Article
- Rat models of human diseases and related phenotypes: a systematic inventory of the causative genes.Journal of biomedical science · 2020Review
- A Mutation inJournal of the American Society of Nephrology : JASN · 2020Article
- Chrm3 Gene and M3 Muscarinic Receptors Contribute to Salt-Sensitive Hypertension.Hypertension (Dallas, Tex. : 1979) · 2018Article
- Elevation of fumarase attenuates hypertension and can result from a nonsynonymous sequence variation or increased expression depending on rat strain.Physiological genomics · 2017Article
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- Shroom3 contributes to the maintenance of the glomerular filtration barrier integrity.Genome research · 2015Article
- SORCS1 is necessary for normal insulin secretory granule biogenesis in metabolically stressed β cells.The Journal of clinical investigation · 2014Article
- Brown Norway chromosome 1 congenic reduces symptoms of renal disease in fatty Zucker rats.PloS one · 2014Article
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Many lines of evidence demonstrate that genetic variability contributes to chronic kidney disease susceptibility in humans as well as rodent models. Little progress has been made in discovering causal kidney disease genes in humans mainly due to genetic complexity. Here, we use a minimal congenic mapping strategy in the FHH (fawn hooded hypertensive) rat to identify Sorcs1 as a novel renal disease candidate gene. We investigated the hypothesis that genetic variation in Sorcs1 influences renal disease susceptibility in both rat and human. Sorcs1 is expressed in the kidney, and knocking out this gene in a rat strain with a sensitized genome background produced increased proteinuria. In vitro knockdown of Sorcs1 in proximal tubule cells impaired protein trafficking, suggesting a mechanism for the observed proteinuria in the FHH rat. Since Sorcs1 influences renal function in the rat, we went on to test this gene in humans. We identified associations between single nucleotide polymorphisms in SORCS1 and renal function in large cohorts of European and African ancestry. The experimental data from the rat combined with association results from different ethnic groups indicates a role for SORCS1 in maintaining proper renal function.
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