ArticleRenal failure2020
Interleukin-22 attenuates renal tubular cells inflammation and fibrosis induced by TGF-β1 through Notch1 signaling pathway.
Article in Renal failure, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- The Role of Aryl Hydrocarbon Receptor-Dependent Signaling Pathway in the Profibrotic Effects of Dioxin-like Compounds in Human Renal Tubular Epithelial Cells.Environment & health (Washington, D.C.) · 2026Article
- Integrated network pharmacology and bioinformatics analysis reveals MME as key target of Notoginsenoside R1 in diabetic nephropathy.BMC complementary medicine and therapies · 2026Article
- rIL-22 Alleviates Severe Acute Pancreatitis and Secondary Multiple Organ Injury Induced by Caerulein in Mice.Inflammation · 2026Article
- Response mechanism of hepatorenal metabolic barrier function to drugs and environmental poisons and intervention strategy of natural products.Frontiers in pharmacology · 2026Review
- Inflammation, Apoptosis, and Fibrosis in Diabetic Nephropathy: Molecular Crosstalk in Proximal Tubular Epithelial Cells and Therapeutic Implications.Current issues in molecular biology · 2025Review
- Blockade of the Notch Pathway by Inhibition of Fucosylation Ameliorates Chondrocyte Inflammation and Extracellular Matrix Degradation.Journal of inflammation research · 2025Article
- Mechanisms Underlying the Impact of Interleukin Family on Acute Kidney Injury: Pathogenesis, Progression, and Therapy.Research (Washington, D.C.) · 2025Review
- The Complex Interplay of TGF-β and Notch Signaling in the Pathogenesis of Fibrosis.International journal of molecular sciences · 2024Review
- The role of Interleukin-22 in severe acute pancreatitis.Molecular medicine (Cambridge, Mass.) · 2024Review
- Secretase promotes AD progression: simultaneously cleave Notch and APP.Frontiers in aging neuroscience · 2024Review
- Therapeutic Potential of Extracts fromPlants (Basel, Switzerland) · 2023Article
- Article
- The progress and prospect of natural components in rhubarb (Frontiers in pharmacology · 2022Review
- Comprehensive Diagnostic Medical System Based on Notch1 Signaling Pathway to Inhibit the Growth of Small-Cell Lung Carcinoma.Journal of healthcare engineering · 2022Article
- The research status and prospect of Periostin in chronic kidney disease.Renal failure · 2020Review
- Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review.Frontiers in pharmacology · 2020Review
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-β1 (TGF-β1) is a crucial factor implicated in the development of renal inflammation and tubulointerstitial fibrosis (TIF). The cytokine interleukin 22 (IL-22) was previously reported to involve in the pathogenesis of chronic inflammatory diseases, however recent studies showed that IL-22 could reduced inflammatory responses and tissue damage. In the present study, we aim to investigate the role and mechanisms of IL-22 in renal tubular cells inflammation and fibrosis induced by TGF-β1. HK-2 cells were treated with TGF-β1 in the presence of IL-22 or the Notch pathway inhibitor dibenzazepine (DBZ) for 48 h. Collagen I (Col I), fibronectin (FN), α-smooth muscle actin (α-SMA), vimentin and E-Cadherin were detected by western blot, proinflammatory factors (TNF-α, IL-6) and chemokines (MCP-1, RANTES) were evaluated by ELISA. Jagged1, Notch1, NICD1, and Hes1 were also detected by western blot. We found TGF-β1 increased the levels of Col I, FN, α-SMA and vimentin in HK-2 cells compared with control, and decreased E-Cadherin level, however, IL-22 restored their expressions partly. IL-22 reduced overexpression of proinflammatory factors (TNF-α, IL-6) and chemokines (MCP-1, RANTES) levels induced by TGF-β1, along with down-regulation of Jagged1, Notch, NICD1 and Hes1. Fibrosis and inflammation in renal tubular cells induced by TGF-β1 could be attenuated by IL-22, and the effects were similar to DBZ treatment. Collectively, our study shows that IL-22 exerts a protective role in renal fibrotic and inflammatory responses induced by TGF-β1
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