ArticleEBioMedicine2019
H19 promote calcium oxalate nephrocalcinosis-induced renal tubular epithelial cell injury via a ceRNA pathway.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- Metabolic changes in kidney stone disease.Frontiers in immunology · 2023Pooled it
- β-carotene attenuates calcium oxalate crystal-induced renal injury through suppression of NF-κB-mediated inflammation.Urolithiasis · 2026Article
- EP3 receptor mediates calcium oxalate kidney stone formation via Ca²⁺/AKT and necroinflammation.Urolithiasis · 2026Article
- Bionic black phosphorus nanosheets confer dual protection against nephrocalcinosis-induced kidney injury via ROS scavenging and NETosis inhibition.Materials today. Bio · 2026Article
- CircRSPRY1 regulates calcium oxalate crystal-induced necrotic apoptosis in renal tubules via miR-21-5p/PTEN.Cell & bioscience · 2026Article
- Unravelling new mechanisms of occurrence and recurrence in calcium nephrolithiasis: the role of epigenetics.World journal of urology · 2026Review
- 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
- Betulinic Acid Attenuates Lipopolysaccharide-Induced Kidney Inflammatory Injury by Suppressing PANoptosis in Weaned Piglets.Veterinary sciences · 2026Article
- Inflammation-related lncRNAs in the regulation of kidney injuries; special emphasis on novel lncRNA-based delivery platforms.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Sirtuin1 mitigation of calcium oxalate nephropathy via enhancing itaconate abundance through reduction of histone trimethylation.Clinical and translational medicine · 2025Article
- Macrophage Reprogramming: Emerging Molecular Therapeutic Strategies for Nephrolithiasis.Biomolecules · 2025Review
- Enhancer Profiling Reveals a Protective Role of RXRα Against Calcium Oxalate-Induced Crystal Deposition and Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Inhibition of NLRP3 alleviates calcium oxalate crystal-induced renal fibrosis and crystal adhesion.Urolithiasis · 2025Article
- Mechanistic studies of CaScientific reports · 2025Article
- The relationship between long noncoding RNAInternational journal of medical sciences · 2025Article
- Epigallocatechin Gallate Attenuates CaOx Crystal-Induced Renal Tubular Injury to Inhibit CaOx Nephrolithiasis via GRP94/PI3K/AKT Signaling.Biomaterials research · 2025Article
- The significance of reactive oxygen species in the formation of calcium oxalate stones and the protective effects of antioxidants on the kidneys.Frontiers in immunology · 2025Review
- The Association of Cell-Free LncH19 and miR-29b Expression with the PI3K/AKT/HIF-1/VEGF Pathway in Patients with Diabetic Nephropathy: In Silico Prediction and Clinical Validation.Current issues in molecular biology · 2024Article
- Identification of key necroptosis-related genes and immune landscape in patients with immunoglobulin A nephropathy.BMC nephrology · 2024Article
- Puerarin alleviates apoptosis and inflammation in kidney stone cells via the PI3K/AKT pathway: Network pharmacology and experimental verification.Journal of cellular and molecular medicine · 2024Article
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntrarenal calcium oxalate (CaOx) crystals induce inflammation and kidney tubular cell injury, which are processes that involve TLR4/NF-κB signalling. A recent genome-wide gene expression profile analysis of Randall's plaques in CaOx stone patients revealed that the expression of the long noncoding RNA H19 was significantly upregulated. However, to date, its role in kidney CaOx stones has not been reported.
methodA Gene Expression Omnibus (GEO) dataset was utilized to analyse gene expression profiles. Luciferase reporter, Western blotting, qRT-PCR, immunofluorescence staining and reactive oxygen species (ROS) assays were employed to study the molecular mechanism of HMGB1/TLR4/NF-κB regulation by H19 and miR-216b. In vitro and in vivo assays were performed to further confirm the proinflammatory and prooxidative stress effects. FINDING: H19 expression was significantly increased and positively correlated with the expression levels of HMGB1, TLR4 and NF-κB in Randall's plaques and glyoxylate-induced CaOx nephrocalcinosis mouse models. H19 interacted with miR-216b and suppressed its expression. Additionally, miR-216b inhibited HMGB1 expression by directly binding its 3'-untranslated region. Moreover, H19 downregulation inhibited HMGB1, TLR4 and NF-κB expression and suppressed CaOx nephrocalcinosis-induced renal tubular epithelial cell injury, NADPH oxidase, and oxidative stress in vivo and in vitro. Interestingly, miR-216b inhibition partially reversed the inhibitory effect of H19 knockdown on HMGB1 expression.
interpretationWe determined that H19 might serve as a facilitator in the process of CaOx nephrocalcinosis-induced oxidative stress and renal tubular epithelial cell injury, and we revealed that the interaction between H19 and miR-216b could exert its effect via the HMGB1/TLR4/NF-κB pathway.
fundingThis work was supported by the National Nature Science Foundation of China (Nos. 8196030190, 8190033175, 81370805, 81470935, 81900645, 81500534, and 81602236).
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