ArticleRenal failure2017
Calcium oxalate crystals induces tight junction disruption in distal renal tubular epithelial cells by activating ROS/Akt/p38 MAPK signaling pathway.
Article in Renal failure, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Metabolic changes in kidney stone disease.Frontiers in immunology · 2023Pooled it
- Article
- Oxalate as an Emerging Contributor to Cardiovascular Disease: Links to Inflammation, Immunity, and Oxidative Stress.Nutrients · 2026Review
- 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
- 2,8-Dihydroxyadenine disrupts epithelial integrity and alters kidney cell phenotype in vitro.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Total flavonoids ofFrontiers in pharmacology · 2026Article
- Hydrogen Sulfide Deficiency Contributes to Tubular Damage and Calcium Oxalate Crystal Formation in Hyperoxaluria Nephropathy: Role of Osteopontin and Tamm-Horsfall Protein.Antioxidants (Basel, Switzerland) · 2025Article
- Effect ofBiomedical reports · 2025Article
- Balancing Stone Prevention and Kidney Function: A Therapeutic Dilemma.Journal of clinical medicine · 2025Review
- Molecular insights into cell signaling pathways in kidney stone formation.Urolithiasis · 2025Review
- Selenium deficiency modulates necroptosis-mediated intestinal inflammation in broiler through the lncRNAWSF27/miRNA1696/GPX3 axis.Journal of animal science · 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
- AI-driven strategies for advancing corneal cell therapy: a promising frontier.Frontiers in medicine · 2025Review
- Ginsenoside Rg1 Alleviates Blood-Milk Barrier Disruption in Subclinical Bovine Mastitis by Regulating Oxidative Stress-Induced Excessive Autophagy.Antioxidants (Basel, Switzerland) · 2024Article
- Machine learning and 4D-LFQ quantitative proteomic analysis explore the molecular mechanism of kidney stone formation.Heliyon · 2024Article
- Effect of Copper and Zinc Ions on Biochemical and Molecular Characteristics of Calcium Oxalate Renal Stones: a Controlled Clinical Study.Biological trace element research · 2024Article
- Tight junction and kidney stone disease.Tissue barriers · 2024Review
- Oxalate‑induced renal pyroptotic injury and crystal formation mediated by NLRP3‑GSDMD signalingMolecular medicine reports · 2023Article
- Inhibitory role of microRNA-484 in kidney stone formation by repressing calcium oxalate crystallization via a VDR/FoxO1 regulator axis.Urolithiasis · 2022Article
- Lipoxin alleviates oxidative stress: a state-of-the-art review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tight junction plays important roles in regulating paracellular transports and maintaining cell polarity. Calcium oxalate monohydrate (COM) crystals, the major crystalline composition of kidney stones, have been demonstrated to be able to cause tight junction disruption to accelerate renal cell injury. However, the cellular signaling involved in COM crystal-induced tight junction disruption remains largely to be investigated. In the present study, we proved that COM crystals induced tight junction disruption by activating ROS/Akt/p38 MAPK pathway. Treating Madin-Darby canine kidney (MDCK) cells with COM crystals induced a substantial increasing of ROS generation and activation of Akt that triggered subsequential activation of ASK1 and p38 mitogen-activated protein kinase (MAPK). Western blot revealed a significantly decreased expression of ZO-1 and occludin, two important structural proteins of tight junction. Besides, redistribution and dissociation of ZO-1 were observed by COM crystals treatment. Inhibition of ROS by N-acetyl-l-cysteine (NAC) attenuated the activation of Akt, ASK1, p38 MAPK, and down-regulation of ZO-1 and occludin. The redistribution and dissociation of ZO-1 were also alleviated by NAC treatment. These results indicated that ROS were involved in the regulation of tight junction disruption induced by COM crystals. In addition, the down-regulation of ZO-1 and occludin, the phosphorylation of ASK1 and p38 MAPK were also attenuated by MK-2206, an inhibitor of Akt kinase, implying Akt was involved in the disruption of tight junction upstream of p38 MAPK. Thus, these results suggested that ROS-Akt-p38 MAPK signaling pathway was activated in COM crystal-induced disruption of tight junction in MDCK cells.
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