ArticleMediators of inflammation2017
Anti-Interleukin-22-Neutralizing Antibody Attenuates Angiotensin II-Induced Cardiac Hypertrophy in Mice.
Article in Mediators of inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Macrophage polarization plasticity in pulmonary fibrosis: a review from pathogenesis to therapeutic targeting.Inflammopharmacology · 2026Review
- Myeloid MyD88 Mediates Macrophage Infiltration and Activation in Ang II-Induced Cardiac Hypertrophy.Journal of cellular and molecular medicine · 2025Article
- Article
- Interleukin-5 alleviates cardiac remodelling via the STAT3 pathway in angiotensin II-infused mice.Journal of cellular and molecular medicine · 2024Article
- Inflammatory proteins mediate male erectile dysfunction via plasma metabolites.Sexual medicine · 2024Article
- Interleukin-22 Alleviates Caerulein-Induced Acute Pancreatitis by Activating AKT/mTOR Pathway.Digestive diseases and sciences · 2024Article
- Promising Therapeutic Treatments for Cardiac Fibrosis: Herbal Plants and Their Extracts.Cardiology and therapy · 2023Review
- Endogenous interleukin-22 prevents cardiac rupture after myocardial infarction in mice.PloS one · 2023Article
- Interleukin-22 Deficiency Reduces Angiotensin II-Induced Aortic Dissection and Abdominal Aortic Aneurysm in ApoE-/- Mice.Oxidative medicine and cellular longevity · 2022Article
- Developmental endothelial locus-1 in cardiovascular and metabolic diseases: A promising biomarker and therapeutic target.Frontiers in immunology · 2022Review
- Article
- Interleukin-22 deficiency alleviates doxorubicin-induced oxidative stress and cardiac injury via the p38 MAPK/macrophage/Fizz3 axis in mice.Redox biology · 2020Article
- Interleukin-22 is elevated in the atrium and plasma of patients with atrial fibrillation and increases collagen synthesis in transforming growth factor-β1-treated cardiac fibroblasts via the JNK pathway.Experimental and therapeutic medicine · 2020Article
- Interleukin-22 Directly Activates Myocardial STAT3 (Signal Transducer and Activator of Transcription-3) Signaling Pathway and Prevents Myocardial Ischemia Reperfusion Injury.Journal of the American Heart Association · 2020Article
- Bazedoxifene Regulates Th17 Immune Response to Ameliorate Experimental Autoimmune myocarditis via Inhibition of STAT3 Activation.Frontiers in pharmacology · 2020Article
- Activation of the STAT3/microRNA-21 pathway participates in angiotensin II-induced angiogenesis.Journal of cellular physiology · 2019Article
- Erratum to "Anti-Interleukin-22-Neutralizing Antibody Attenuates Angiotensin II-Induced Cardiac Hypertrophy in Mice".Mediators of inflammation · 2018Article
- Recent Developments on the Crosstalk Between STAT3 and Inflammation in Heart Function and Disease.Frontiers in immunology · 2018Review
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInterleukin- (IL-) 22 is considered a proinflammatory cytokine. Recent evidence has demonstrated that it plays a role in cardiovascular diseases. In the recent study, we investigate whether IL-22 is involved in cardiac hypertrophy.
methodsAngiotensin II was used to build hypertrophy model and the IL-22 and IL-22 receptor 1 (IL-22R1) levels in heart tissue were measured. In addition, angiotensin II-treated mice received an injection of anti-IL-22-neutralizing antibody (nAb) to investigate the effects of IL-22 nAb on myocardial hypertrophy, cardiac function, and cardiac fibrosis; the activation of the signaling pathway and the prohypertrophic inflammatory cytokine mRNA levels was detected. Furthermore, the effect of IL-22 nAb on angiotensin II-induced hypertrophy in vitro was also determined.
resultsIL-22 and IL-22R1 levels were significantly increased after angiotensin II infusion. Anti-IL-22 nAb significantly alleviated the severity of hypertrophy, prevented systolic and diastolic abnormalities, reduced cardiac fibrosis, STAT3 and ERK phosphorylation, and downregulated the mRNA expression of IL-17, IL-6, IL-1
conclusionOur data demonstrated that neutralization of IL-22 alleviated angiotensin II-induced cardiac hypertrophy. The downregulation of IL-22 may be a novel therapeutic strategy to prevent cardiac hypertrophy.
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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.