ArticlePloS one2013
Interleukin-19 mediates tissue damage in murine ischemic acute kidney injury.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Mechanisms Underlying the Impact of Interleukin Family on Acute Kidney Injury: Pathogenesis, Progression, and Therapy.Research (Washington, D.C.) · 2025Review
- Exploring the JAK/STAT Signaling Pathway in Hepatocellular Carcinoma: Unraveling Signaling Complexity and Therapeutic Implications.International journal of molecular sciences · 2023Review
- Interleukin-19 Aggravates Pulmonary Fibrosis via Activating Fibroblast through TGF-Mediators of inflammation · 2022Article
- Recombinant Interleukin-19 Suppresses the Formation and Progression of Experimental Abdominal Aortic Aneurysms.Journal of the American Heart Association · 2021Article
- Review
- Interleukin-24 regulates mucosal remodeling in inflammatory bowel diseases.Journal of translational medicine · 2021Article
- Immunopathobiology and therapeutic targets related to cytokines in liver diseases.Cellular & molecular immunology · 2021Review
- Interleukin-19 enhances cytokine production induced by lipopolysaccharide and inhibits cytokine production induced by polyI:C in BALB/c mice.The Journal of veterinary medical science · 2020Article
- Characterization of IL-19, -20, and -24 in acute and chronic kidney diseases reveals a pro-fibrotic role of IL-24.Journal of translational medicine · 2020Article
- IL-20 in Acute Kidney Injury: Role in Pathogenesis and Potential as a Therapeutic Target.International journal of molecular sciences · 2020Review
- Blocking IL-19 Signaling Ameliorates Allergen-Induced Airway Inflammation.Frontiers in immunology · 2019Article
- Interleukin-19 is cardioprotective in dominant negative cyclic adenosine monophosphate response-element binding protein-mediated heart failure in a sex-specific manner.World journal of cardiology · 2017Article
- Acute kidney injury during a pediatric sickle cell vaso-occlusive pain crisis.Pediatric nephrology (Berlin, Germany) · 2017Article
- Article
- Preliminary expression profile of cytokines in brain tissue of BALB/c mice with Angiostrongylus cantonensis infection.Parasites & vectors · 2015Article
- Augmenter of liver regeneration attenuates inflammation of renal ischemia/reperfusion injury through the NF-kappa B pathway in rats.International urology and nephrology · 2015Article
- Fibrosis Related Inflammatory Mediators: Role of the IL-10 Cytokine Family.Mediators of inflammation · 2015Review
- The IL-20 subfamily of cytokines--from host defence to tissue homeostasis.Nature reviews. Immunology · 2014Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation and renal tubular injury are major features of acute kidney injury (AKI). Many cytokines and chemokines are released from injured tubular cells and acts as proinflammatory mediators. However, the role of IL-19 in the pathogenesis of AKI is not defined yet. In bilateral renal ischemia/reperfusion injury (IRI)-induced and HgCl2-induced AKI animal models, real-time quantitative (RTQ)-PCR showed that the kidneys, livers, and lungs of AKI mice expressed significantly higher IL-19 and its receptors than did sham control mice. Immunohistochemical staining showed that IL-19 and its receptors were strongly stained in the kidney, liver, and lung tissue of AKI mice. In vitro, IL-19 upregulated MCP-1, TGF-β1, and IL-19, and induced mitochondria-dependent apoptosis in murine renal tubular epithelial M-1 cells. IL-19 upregulated TNF-α and IL-10 in cultured HepG2 cells, and it increased IL-1β and TNF-α expression in cultured A549 cells. In vivo, after renal IRI or a nephrotoxic dose of HgCl2 treatment, IL-20R1-deficient mice (the deficiency blocks IL-19 signaling) showed lower levels of blood urea nitrogen (BUN) in serum and less tubular damage than did wild-type mice. Therefore, we conclude that IL-19 mediates kidney, liver, and lung tissue damage in murine AKI and that blocking IL-19 signaling may provide a potent therapeutic strategy for treating AKI.
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