ArticleJournal of the American Society of Nephrology : JASN2014
IL-22 ameliorates renal ischemia-reperfusion injury by targeting proximal tubule epithelium.
Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
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Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.
- Macrophages in Renal Injury, Repair, Fibrosis Following Acute Kidney Injury and Targeted Therapy.Frontiers in immunology · 2022Pooled it
- Anti-ANGPTL3 antibody and IL-22 fusion protein mitigate nephrotic syndrome via mitochondrial protection, anti-apoptosis, and autophagy suppression.Antibody therapeutics · 2026Article
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- [Eurycomanone inhibits renal ischemia/reperfusion-induced mitochondrial dysfunction and inflammation in mice by binding to STAT3 to inhibit its phosphorylation].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- rIL-22 Alleviates Severe Acute Pancreatitis and Secondary Multiple Organ Injury Induced by Caerulein in Mice.Inflammation · 2026Article
- Article
- Multifaceted mechanisms of unconventional T cells in ischemia-reperfusion injury.Frontiers in immunology · 2026Review
- Laptm4a mediates renal ischemia-reperfusion injury by regulating the UNC5B-AKT/mTOR signaling pathway.Frontiers in immunology · 2026Article
- ILC imbalance - a new piece in the gut-kidney axis puzzle.Frontiers in immunology · 2026Review
- An Update on IL-22 Therapies in Alcohol-Associated Liver Disease and Beyond.The American journal of pathology · 2026Review
- Myeloid Cells in Acute Kidney Injury.Seminars in nephrology · 2025Review
- Evaluating IL22RA1 expression as a predictive indicator in human colon cancer progression.BMC cancer · 2025Article
- IL-22 Attenuates Pressure Overload-Induced Heart Failure and Inflammation.Journal of cardiovascular translational research · 2025Article
- Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury.The Journal of clinical investigation · 2025Review
- Mechanisms Underlying the Impact of Interleukin Family on Acute Kidney Injury: Pathogenesis, Progression, and Therapy.Research (Washington, D.C.) · 2025Review
- Protective effects of pioglitazone in renal ischemia-reperfusion injury (RIRI): focus on oxidative stress and inflammation.Clinical and experimental nephrology · 2024Review
- Traditional Chinese Medicine and renal regeneration: experimental evidence and future perspectives.Chinese medicine · 2024Review
- IL-22 is secreted by proximal tubule cells and regulates DNA damage response and cell death in acute kidney injury.Kidney international · 2024Article
- Syndecan-1 shedding destroys epithelial adherens junctions through STAT3 after renal ischemia/reperfusion injury.iScience · 2023Article
- Interleukin-22 promotes the proliferation and migration of hepatocellular carcinoma cells via the phosphoinositide 3-kinase (PI3K/AKT) signaling pathway.Molecular biology reports · 2023Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
IL-22 is an epithelial cell survival cytokine that is currently under development for the treatment of acute liver damage. Here, we used a mouse model of renal ischemia/reperfusion (I/R) injury to investigate whether IL-22 has therapeutic potential for the treatment of AKI. The action of IL-22 is mediated by binding to IL-22R1 and leads to STAT3 activation. Under physiologic conditions, renal expression of IL-22R1 was detected only in the brush border of the renal proximal tubular epithelial cells (RPTECs). Renal I/R elevated serum IL-22 levels slightly but did not induce STAT3 phosphorylation in RPTECs. IL-22-deficient mice had slightly increased I/R-induced injury compared with wild-type mice. In contrast, treatment with IL-22 or overexpression of IL-22 by either gene targeting (IL-22 transgenic mice) or administration of adenovirus expressing IL-22 increased STAT3 phosphorylation in RPTECs, ameliorated I/R-induced renal inflammation and tubular cell injury, and preserved renal functions. Overexpression of IL-22 increased the phosphorylation of STAT3 and Akt, upregulated antiapoptotic genes (e.g., Bcl-2), and downregulated proapoptotic genes (e.g., Bad) in the kidneys of mice subjected to I/R. Notably, phosphorylation of Akt increased and expression of Bad decreased in proximal tubular cells under these conditions. Furthermore, compared with wild-type mice, IL-22 transgenic mice had increased survival rates, whereas IL-22-deficient mice had reduced survival rates after I/R injury. In summary, renal expression of IL-22R1 is restricted to RPTECs, and treatment with IL-22 protects against renal I/R injury by activating STAT3 and AKT, suggesting that IL-22 has therapeutic potential for the treatment of AKI.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.