ArticleUrolithiasis2021
Regulation of endoplasmic reticulum stress on the damage and apoptosis of renal tubular epithelial cells induced by calcium oxalate crystals.
Article in Urolithiasis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Role of ROS-Induced NLRP3 Inflammasome Activation in the Formation of Calcium Oxalate Nephrolithiasis.Frontiers in immunology · 2022Pooled it
- Apigenin activates AKT1 to coordinate MTOR-mediated anti-apoptosis and FOXO3-driven antioxidant defense in calcium oxalate nephropathy.International journal of surgery (London, England) · 2026Article
- Paeoniflorin alleviates nephrolithiasis by targeting serpine1 and inhibiting the NF-κB signaling pathway.Urolithiasis · 2026Article
- Article
- Identification of Key Genes Associated with Endoplasmic Reticulum Stress in Calcium Oxalate Kidney Stones.Genes · 2025Article
- CHAC1 Mediates Endoplasmic Reticulum Stress-Dependent Ferroptosis in Calcium Oxalate Kidney Stone Formation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Premature renal epithelial cell senescence promoted by LXN/Rps3/p53 signaling pathway activation increases calcium oxalate crystal deposition by altering macrophage polarization.Frontiers in immunology · 2025Article
- Article
- Article
- Machine learning and 4D-LFQ quantitative proteomic analysis explore the molecular mechanism of kidney stone formation.Heliyon · 2024Article
- SulfatedPharmaceuticals (Basel, Switzerland) · 2024Article
- Cell death‑related molecules and targets in the progression of urolithiasis (Review).International journal of molecular medicine · 2024Review
- Understanding formation processes of calcareous nephrolithiasis in renal interstitium and tubule lumen.Journal of cellular and molecular medicine · 2024Review
- Ferroptosis and its emerging role in kidney stone formation.Molecular biology reports · 2024Review
- Epitranscriptomic profiling of m6A RNA methylation in renal epithelial tubular cells stimulated with calcium oxalate crystals through microarray analysis.Urolithiasis · 2023Article
- Proteomics and transcriptomics profiling reveals distinct aspects of kidney stone related genes in calculi rats.BMC genomics · 2023Article
- The mechanism of programmed death and endoplasmic reticulum stress in pulmonary hypertension.Cell death discovery · 2023Review
- Drug repurposing screens to identify potential drugs for chronic kidney disease by targeting prostaglandin E2 receptor.Computational and structural biotechnology journal · 2023Article
- Carboxymethylation ofOxidative medicine and cellular longevity · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
This study aimed to observe whether calcium oxalate (CaOx) crystals can induce the activation of endoplasmic reticulum (ER) stress in human renal cortex proximal tubule epithelial (HK-2) cells and to explore the regulatory of ER stress on the damage and apoptosis of HK-2 cells induced by CaOx crystals. We detected the optimal CaOx crystal concentration and intervention time by Western blot. ER stress modifiers tunicamycin (TM) and 4-phenylbutyric acid (4-PBA) were used to regulate the ER stress of HK-2 cells. The activities of ER stress marker proteins GRP78 and CHOP were evaluated by Western blot and immunohistochemistry. Western blot and TUNEL staining were used to detect cell apoptosis. We observed cell-crystal adhesion with an optical microscope. Lactate dehydrogenase (LDH) test kit and IL-1β enzyme-linked immunosorbent assay kit were used to detect and evaluate HK-2 cell damage. We found that the expression of ER stress marker proteins GRP78 and CHOP gradually increased with the increase in CaOx crystal concentration and intervention time and reached the maximum at 2.0 mmol/L and 24 h. The use of ER stress modifiers TM and 4-PBA can effectively regulate the ER stress level induced by CaOx crystals, and the level of apoptosis is positively correlated with the level of ER stress. 4-PBA pretreatment remarkably reduced cell-crystal adhesion and the secretions of IL-1β and LDH, whereas the results of TM pretreatment were the opposite. In summary, the damage and apoptosis of HK-2 cells induced by CaOx crystals are closely related to the level of ER stress. Inhibiting the ER stress of HK-2 cells can substantially reduce the cell damage and apoptosis induced by CaOx crystals.
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