ArticleInternational journal of endocrinology2021
PERK-Dependent Activation of the JAK2/STAT3 Pathway Contributes to High Glucose-Induced Extracellular Matrix Deposition in Renal Tubular Epithelial Cells.
Article in International journal of endocrinology, 2021. 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, 14 citations in OpenAlex.
- Analysis of potential targets of 20S-protopanaxadiol on diabetic nephropathy based on network pharmacology, molecular docking, and experimental validation.Renal failure · 2025Article
- Integrin-Specific Signaling Drives ER Stress-Dependent Atherogenic Endothelial Activation.bioRxiv : the preprint server for biology · 2025Article
- Advances in Traditional Chinese Medicine research in diabetic kidney disease treatment.Pharmaceutical biology · 2024Review
- The mRNA and microRNA Landscape of the Blastema Niche in Regenerating Newt Limbs.International journal of molecular sciences · 2024Article
- Integrated UPLC-ESI-MS/MS, network pharmacology, and transcriptomics to reveal the material basis and mechanism of Schisandra chinensis Fruit Mixture against diabetic nephropathy.Frontiers in immunology · 2024Article
- TIAR and FMRP shape pro-survival nascent proteome of leukemia cells in the bone marrow microenvironment.iScience · 2023Article
- Endoplasmic Reticulum Stress in Renal Cell Carcinoma.International journal of molecular sciences · 2023Review
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough the deposition of extracellular matrix (ECM) is critical leading to tubular damage in diabetic kidney disease (DKD), the mechanism still remains unclear. The purpose of this study was to demonstrate a role for protein kinase R-like endoplasmic reticulum kinase (PERK) (a protein located in the endoplasmic reticulum membrane) in this pathologic process.
methodsNRK-52E cells were grown in the media containing different concentrations of glucose or thapsigargin for different durations. Cells were subsequently incubated with or without AG490, a selective inhibitor of Janus kinase 2 (JAK2) or GSK2606414 (a selective PERK inhibitor). We evaluated the production of TGF-
resultsWe showed that the increased phosphorylation of JAK2 and STAT3 was accompanied by overexpression of TGF-
conclusionOur data indicated that the ECM accumulation induced by high glucose arouse via the PERK-dependent JAK2/STAT3-signaling pathway in renal tubular epithelial cells.
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