ArticleLaboratory investigation; a journal of technical methods and pathology2019
Protective effect and mechanism of IL-10 on renal ischemia-reperfusion injury.
Article in Laboratory investigation; a journal of technical methods and pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- The Effect of Interleukin-10 Immunotherapy on Renal Ischemia-Reperfusion Injury: A Systematic Review and Meta-Analysis of Preclinical Studies.International journal of molecular sciences · 2024Pooled it
- The NRF2 stimulating agent, tin protoporphyrin, activates protective cytokine pathways in healthy human subjects and in patients with chronic kidney disease.Physiological reports · 2020Trial
- Multifaceted mechanisms of unconventional T cells in ischemia-reperfusion injury.Frontiers in immunology · 2026Review
- Acute kidney injury disrupts cardiac remodeling via SerpinA3N.bioRxiv : the preprint server for biology · 2025Article
- ST2 + T-Regulatory Cells in Renal Inflammation and Fibrosis after Ischemic Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Article
- Interleukin-10: Genetic and biochemical prediction of sepsis-induced acute kidney injury in critically ill patients in intensive care unit: A cross-sectional study.Journal of the Chinese Medical Association : JCMA · 2024Article
- Innovative hydrogel-based therapies for ischemia-reperfusion injury： bridging the gap between pathophysiology and treatment.Materials today. Bio · 2024Review
- [Acute kidney injury after laparoscopic radical nephrectomy: role of the renin-angiotensin system and the predictive value of its activation status].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Morphofunctional Features of Glomeruli and Nephrons After Exposure to Electrons at Different Doses: Oxidative Stress, Inflammation, Apoptosis.Current issues in molecular biology · 2024Article
- Interleukin-10 enhances recruitment of immune cells in the neonatal mouse model of obstructive nephropathy.Scientific reports · 2024Article
- Molecular Challenges and Opportunities in Climate Change-Induced Kidney Diseases.Biomolecules · 2024Review
- Renal tubular epithelial cells are constitutive non-cognate stimulators of resident T cells.Cell reports · 2023Article
- Myrrh Essential Oil Mitigates Renal Ischemia/Reperfusion-Induced Injury.Current issues in molecular biology · 2023Article
- Pharmacological functions of salidroside in renal diseases: facts and perspectives.Frontiers in pharmacology · 2023Review
- Ferroptosis and renal fibrosis: A new target for the future (Review).Experimental and therapeutic medicine · 2023Review
- Review
- Sufentanil promotes autophagy and improves ischemiaZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022Article
- Network Pharmacology-Based Exploration of the Therapeutic Mechanisms of Cordyceps cicadae in Renal Ischemia/Reperfusion.Annals of transplantation · 2022Article
- Targeting Interleukin-10 Restores Graft Microvascular Supply and Airway Epithelium in Rejecting Allografts.International journal of molecular sciences · 2022Article
- Protective effects of mefunidone on ischemia-reperfusion injury/Folic acid-induced acute kidney injury.Frontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin (IL)-10, a cytokine with anti-inflammatory effects, is produced by blood cells and cells of various organs. Ischemia-reperfusion injury (IRI) is a systemic inflammatory disease caused by a systemic circulation of pro-inflammatory cytokines and chemokines produced from blood cells or organs damaged by ischemia. Apoptosis, a key event after IRI, is correlated with the degree of injury. Here we investigated the effects and mechanism of IL-10 in renal IRI. Compared to wild-type (WT) mice with a renal IRI, IL-10 knockout (IL-10 KO) mice with IRI demonstrated decreased renal function as represented by blood urea nitrogen and serum creatinine, upregulated early acute kidney injury (AKI) biomarkers such as kidney injury molecule-1 (Kim-1), increased mRNA expression of the pro-inflammatory cytokines IL-1β, IL-6, and IL-18 and a chemokine (regulated on activation, normal T cell expressed and secreted; RANTES), and increased expression of the pro-apoptosis factors Bax and cleaved caspase-3. When tubular epithelial cells (TECs) from IL-10 KO mice were put in a hypoxic state and added with recombinant IL-10, their expression of Bax decreased. Our findings demonstrated that IL-10 suppressed the production of pro-inflammatory cytokines, renal dysfunction, and the expression of pro-apoptosis factors after IRI.
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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.