ArticleUrolithiasis2024
A high-calcium environment induced ectopic calcification of renal interstitial fibroblasts via TFPI-2-DCHS1-ALP/ENPP1 axis to participate in Randall's plaque formation.
Article in Urolithiasis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Novel insights into the role of the renal interstitial microenvironment in Randall's plaque formation (Review).International journal of molecular medicine · 2026Review
- Targeting GLS and LPIN2 in renal fibroblasts: potential therapeutic targets for kidney stone disease identified by integrated multi-omics analysis.Urolithiasis · 2026Article
- Article
- FASLG Derived from Fibroblasts in Hydroxyapatite-Rich Microenvironment Induces Urothelial Anoikis to Trigger Randall's Plaque Exposure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cell Calcification Models and Their Implications for Medicine and Biomaterial Research.Advanced healthcare materials · 2026Review
- M2 Macrophages Attenuate AQP2Research (Washington, D.C.) · 2026Article
- Reassessing the Role of Tissue Factor Pathway Inhibitor 2 in Neoplastic and Non-Neoplastic Lesions.Cancers · 2025Review
- Epigallocatechin Gallate Attenuates CaOx Crystal-Induced Renal Tubular Injury to Inhibit CaOx Nephrolithiasis via GRP94/PI3K/AKT Signaling.Biomaterials research · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Randall's plaques (RP) serve as anchoring sites for calcium oxalate (CaOx) stones, but the underlying mechanism remains unclear. Renal interstitium with a high-calcium environment is identified as pathogenesis of RP formation where the role of human renal interstitial fibroblasts (hRIFs) was highlighted. Our study aims to elucidate the potential mechanism by which a high-calcium environment drives ectopic calcification of hRIFs to participate in RP formation. Alizarin Red staining demonstrated calcium nodules in hRIFs treated with high-calcium medium. Utilizing transcriptome sequencing, tissue factor pathway inhibitor-2 (TFPI-2) was found to be upregulated in high-calcium-induced hRIFs and RP tissues, and TFPI-2 promoted high-calcium-induced calcification of hRIFs. Subsequently, the downstream regulator of TFPI2 was screened by transcriptome sequencing analysis of hRIFs with TFPI-2 knockdown or overexpressed. Dachsous Cadherin Related 1 (DCHS1) knockdown was identified to suppress the calcification of hRIFs enhanced by TFPI-2. Further investigation revealed that TFPI-2/DCHS1 axis promoted high-calcium-induced calcification of hRIFs via disturbing the balance of ENPP1/ALP activities, but without effect on the canonical osteogenic markers, such as osteopontin (OPN), osteogenic factors runt-related transcription factor 2 (RUNX2), bone morphogenetic protein 2 (BMP2). In summary, our study mimicked the high-calcium environment observed in CaOx stone patients with hypercalciuria, and discovered that the high-calcium drove ectopic calcification of hRIFs via a novel TFPI-2-DCHS1-ALP/ENPP1 pathway rather than adaption of osteogenic phenotypes to participate in RP formation.
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Registered trials
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