ArticleGenes & diseases2022
Vitamin D receptor (VDR) contributes to the development of hypercalciuria by sensitizing VDR target genes to vitamin D in a genetic hypercalciuric stone-forming (GHS) rat model.
Article in Genes & diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Unravelling the Complex Relationship between Diet and Nephrolithiasis: The Role of Nutrigenomics and Nutrigenetics.Nutrients · 2022Pooled it
- Unravelling new mechanisms of occurrence and recurrence in calcium nephrolithiasis: the role of epigenetics.World journal of urology · 2026Review
- Review
- Systematic proteomics analysis of lysine acetylation reveals critical features of renal proteins in kidney calculi formation.PloS one · 2026Article
- Vitamin D/VDR Signaling and Programmed Cell Death in Sepsis-Associated Organ Injury: Evidence from Sepsis and Related Disease Models.Journal of inflammation research · 2026Review
- Association of single nucleotide genetic polymorphisms of vitamin D receptor and calcium-sensitive receptor with calcium-containing kidney stones in Chinese Dai populations: a prospective multi-center study.International urology and nephrology · 2024Article
- Roles of distinct nuclear receptors in diabetic cardiomyopathy.Frontiers in pharmacology · 2024Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human idiopathic hypercalciuria (IH) is the most common cause of calcium oxalate nephrolithiasis with perturbed calcium metabolism with increased bone resorption and decreased renal calcium reabsorption, which can be phenotype-copied in the genetic hypercalciuric stone-forming (GHS) rat model. We previously demonstrated that high VDR expression plays important roles in the development of hypercalciuria in the GHS rats. However, the underlying mechanism through which VDR impact hypercalciuria development remains to be fully understood. Here, we sought to determine how VDR regulated its target genes that are implicated in calcium homeostasis and potentially hypercalciuria. We found that VDR expression in the GHS rats was elevated in the calcium transporting tissues, as well as in the thymus and prostate, but not in lung, brain, heart, liver and spleen, when compared with control SD rats. Snail expression in the GHS rats was significantly downregulated in kidney, intestine, thymus and testis. Intraperitoneal injection of 1,25(OH)
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