ArticleRedox biology2020
Interleukin-22 deficiency alleviates doxorubicin-induced oxidative stress and cardiac injury via the p38 MAPK/macrophage/Fizz3 axis in mice.
Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Decoding the Cardiac Immune Microenvironment and Fibroblast Crosstalk in Radiotherapy Combined with Immunotherapy-Induced Cardiac Fibrosis Based on Single-Cell Transcriptomic Analysis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- SLAMF7 Restrains Pro-Inflammatory Macrophage Activation to Counteract Doxorubicin-Induced Cardiotoxicity.JACC. Basic to translational science · 2025Article
- The reciprocal regulation between autophagy and IL-22: implications for immunity and therapy.Clinical and experimental medicine · 2025Review
- Deficiency of synaptotagmin-1 aggravates pressure overload-induced cardiac hypertrophy and dysfunction via the p38 MAPK signaling pathway in mice.Human cell · 2025Article
- Knockdown of EBP1 promotes doxorubicin-induced apoptosis in renal clear cell carcinoma cells through activation of the p38/HIF-1α pathway.Oncology letters · 2025Article
- Sodium-glucose cotransporter 2 inhibitors and the cancer patient: from diabetes to cardioprotection and beyond.Basic research in cardiology · 2025Review
- The AhR/IL-22 axis in chronic gut inflammation: unraveling mechanisms and therapeutic prospects.Frontiers in immunology · 2025Review
- Article
- A longitudinal evaluation of oxidative stress - mitochondrial dysfunction - ferroptosis genes in anthracycline-induced cardiotoxicity.BMC cardiovascular disorders · 2024Article
- IL-30 protects against sepsis-induced myocardial dysfunction by inhibiting pro-inflammatory macrophage polarization and pyroptosis.iScience · 2023Article
- A bifunctional fusion protein protected against diabetic nephropathy by suppressing NLRP3 activation.Applied microbiology and biotechnology · 2023Article
- A novel peptide HSP-17 ameliorates oxidative stress injury and apoptosis in H9c2 cardiomyocytes by activating the PI3K/Akt pathway.Annals of translational medicine · 2022Article
- The Innate Immune System in Cardiovascular Diseases and Its Role in Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2022Review
- Interleukin-22 protects from endotoxemia by inducing suppressive F4/80BMC immunology · 2022Article
- IL-12p40 deletion aggravates lipopolysaccharide-induced cardiac dysfunction in mice.Frontiers in cardiovascular medicine · 2022Article
- Interleukin-22: a potential therapeutic target in atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2021Review
- Anti-Interleukin-16-Neutralizing Antibody Attenuates Cardiac Inflammation and Protects against Cardiac Injury in Doxorubicin-Treated Mice.Mediators of inflammation · 2021Article
- Guilingji Protects Against Spermatogenesis Dysfunction From Oxidative Stress via Regulation of MAPK and Apoptotic Signaling Pathways in Immp2l Mutant Mice.Frontiers in pharmacology · 2021Article
- Resolvin D1 Attenuates Doxorubicin-Induced Cardiotoxicity by Inhibiting Inflammation, Oxidative and Endoplasmic Reticulum Stress.Frontiers in pharmacology · 2021Article
- Anti-Interleukin-16 Neutralizing Antibody Treatment Alleviates Sepsis-Induced Cardiac Injury and Dysfunction via the Nuclear Factor Erythroid-2 Related Factor 2 Pathway in Mice.Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
- Erratum issued
- Retracted
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several interleukin (IL) family members have been demonstrated to be involved in doxorubicin (DOX)-induced cardiac injury. This study aimed to investigate the role of IL-22 in DOX-induced cardiac injury and explore its possible mechanisms. In this study, mice were given DOX, and the cardiac expression and sources of IL-22 were determined. Then, IL-22 was knocked out to observe the effects on DOX-induced cardiac injury in mice. In addition, the p38 mitogen-activated protein kinase (MAPK) pathway was inhibited, macrophages were depleted and adoptively transferred, and Fizz3 was up-regulated in mice to explore the mechanisms. The results showed that cardiac IL-22 expression was significantly increased by DOX treatment and was mostly derived from cardiac macrophages. IL-22 knockout significantly reduced cardiac vacuolization and the expression of cardiomyocyte injury markers in both serum and left ventricular tissue and improved cardiac function in DOX-treated mice. In addition, IL-22 knockout reversed DOX-induced cardiac M1 macrophage/M2 macrophage imbalance, reduced oxidative stress and protected against cardiomyocyte apoptosis. p38 MAPK pathway inhibition with SB203580 and macrophage depletion further alleviated the above effects in DOX-treated IL-22-knockout mice. The effects were stronger IL-22-knockout mice with adoptive transfer of WT macrophages than in those with adoptive transfer of IL-22-knockout macrophages. Furthermore, increasing the expression of Fizz3 reduced cardiomyocyte apoptosis and alleviated cardiac dysfunction. Our results may suggest that IL-22 knockout alleviate DOX-induced oxidative stress and cardiac injury by inhibiting macrophage differentiation and thereby increasing the expression of Fizz3. Reductions in IL-22 expression may be beneficial for clinical chemotherapy in tumor patients.
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