ArticleJournal of the American Society of Nephrology : JASN2017
Genome-Wide Gene Expression Profiling of Randall's Plaques in Calcium Oxalate Stone Formers.
Article in Journal of the American Society of Nephrology : JASN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 2 of them syntheses that pooled it.
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Who cites it
110 citing papers in PubMed, 2 syntheses or guidelines pooled it, 141 citations in OpenAlex.
- Role of ROS-Induced NLRP3 Inflammasome Activation in the Formation of Calcium Oxalate Nephrolithiasis.Frontiers in immunology · 2022Pooled it
- Macrophage Function in Calcium Oxalate Kidney Stone Formation: A Systematic Review of Literature.Frontiers in immunology · 2021Pooled it
- Novel insights into the role of the renal interstitial microenvironment in Randall's plaque formation (Review).International journal of molecular medicine · 2026Review
- A Mitochondrial-Related Gene Signature for Diagnosis and Immune Microenvironment Modulation in Lung Cancer and Venous Thromboembolism.World journal of oncology · 2026Article
- Neutrophil Secretory Proteins Inhibit Calcium Oxalate Crystallisation and Crystal Growth, but Promote Crystal Aggregation.Immunology · 2026Article
- Article
- Expression analysis of epithelial membrane protein 1 (EMP1) gene in kidney stone patients.International urology and nephrology · 2026Article
- The roles of free-fatty acid receptors in the pathophysiology of renal disorders.The Journal of pharmacology and experimental therapeutics · 2026Review
- ACAA1 mediates arachidonic acid dysregulation and membrane phospholipid remodeling to promote crystal-cell adhesion and ferroptosis susceptibility in calcium oxalate kidney stone.Journal of pharmaceutical analysis · 2026Article
- Clusterin elaborated by renal tubular epithelial cells under high oxalate stress serves as a matrix protein to facilitate kidney stone formation.Cellular and molecular life sciences : CMLS · 2026Article
- Inflammation-induced osteogenic signaling promotes calcium phosphate crystal formation in kidneys via MAPK, NF-κB, and smad pathways.Frontiers in cell and developmental biology · 2026Article
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- Article
- Regulated Cell Death in Calcium Oxalate Stone Disease: From Tubular Epithelial Injury to Inflammatory Amplification.Journal of inflammation research · 2026Review
- The role of inflammation and ROS in CaOx kidney stones.European journal of medical research · 2025Review
- Identification of Key Genes Associated with Endoplasmic Reticulum Stress in Calcium Oxalate Kidney Stones.Genes · 2025Article
- A novel synbiotic formulation prevents calcium oxalate stones by restoring gut microbiota homeostasis.BMC microbiology · 2025Article
- Differential expression of glycolysis-related genes and their potential immune mechanisms in acute myocardial infarction.Journal of cardiothoracic surgery · 2025Article
- Differential expression of glucose metabolism and circadian rhythm-related genes in patients with acute myocardial infarction and their clinical significance.Scientific reports · 2025Article
- Scanning electron microscopy and energy dispersive spectroscopy of Randall's plaque stones: an unexpected finding of monosodium urate crystals.Urolithiasis · 2025Article
50 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Randall plaques (RPs) can contribute to the formation of idiopathic calcium oxalate (CaOx) kidney stones; however, genes related to RP formation have not been identified. We previously reported the potential therapeutic role of osteopontin (OPN) and macrophages in CaOx kidney stone formation, discovered using genome-recombined mice and genome-wide analyses. Here, to characterize the genetic pathogenesis of RPs, we used microarrays and immunohistology to compare gene expression among renal papillary RP and non-RP tissues of 23 CaOx stone formers (SFs) (age- and sex-matched) and normal papillary tissue of seven controls. Transmission electron microscopy showed OPN and collagen expression inside and around RPs, respectively. Cluster analysis revealed that the papillary gene expression of CaOx SFs differed significantly from that of controls. Disease and function analysis of gene expression revealed activation of cellular hyperpolarization, reproductive development, and molecular transport in papillary tissue from RPs and non-RP regions of CaOx SFs. Compared with non-RP tissue, RP tissue showed upregulation (˃2-fold) of LCN2, IL11, PTGS1, GPX3, and MMD and downregulation (0.5-fold) of SLC12A1 and NALCN (P<0.01). In network and toxicity analyses, these genes associated with activated mitogen-activated protein kinase, the Akt/phosphatidylinositol 3-kinase pathway, and proinflammatory cytokines that cause renal injury and oxidative stress. Additionally, expression of proinflammatory cytokines, numbers of immune cells, and cellular apoptosis increased in RP tissue. This study establishes an association between genes related to renal dysfunction, proinflammation, oxidative stress, and ion transport and RP development in CaOx SFs.
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