ArticleBasic research in cardiology2017
IL-10 improves cardiac remodeling after myocardial infarction by stimulating M2 macrophage polarization and fibroblast activation.
Article in Basic research in cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 273 papers, 3 of them syntheses that pooled it.
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Who cites it
273 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Cardiovascular System is Influenced by Skeletal Muscle-derived Extracellular Vesicles, Myokines and MicroRNAs Based on Interorgan Communication: A Systematic Review.International journal of medical sciences · 2025Pooled it
- 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
- Cardiac repair after myocardial infarction: A two-sided role of inflammation-mediated.Frontiers in cardiovascular medicine · 2022Pooled it
- Lactylation at the metabolic-epigenetic interface in cardiovascular diseases: context-dependent mechanisms and translational roadmap.Journal of advanced research · 2026Review
- Roles of inflammation and metabolic dysfunction in cardiovascular diseases: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- Spatiotemporal Nanotherapy After Myocardial Infarction: Targeting the Inflammatory-to-reparative Transition With Extracellular Vesicles and Engineered Nanoparticles.Cardiovascular drugs and therapy · 2026Review
- Antiviral innate immunity in myocarditis: mechanisms and emerging therapeutics.Experimental & molecular medicine · 2026Review
- Lactylation: A central metabolic-epigenetic driver of sepsis-associated acute kidney injury.Molecular biology reports · 2026Review
- Harnessing macrophage signaling pathways and scalable engineering for next-generation immunotherapies.Signal transduction and targeted therapy · 2026Review
- Metabolic regulation of macrophage polarization in myocardial infarction: from mechanisms to targeted therapies.Journal of translational medicine · 2026Review
- Regulation of acute myocardial infarction by CircTMCC1 through mitochondrial dysfunction and AMPK/mTOR-driven M1 macrophage polarization: role in QFR assessment.Cell death discovery · 2026Article
- IL-15 aggravates cardiac ischemic injury via impairing macrophage efferocytosis and driving inflammation.Journal of Zhejiang University. Science. B · 2026Article
- Immuno-instructive biomaterials for coronary artery disease and myocardial infarction repair.Journal of materials science. Materials in medicine · 2026Review
- Ferroptosis and macrophage polarization: mechanisms, interplay, and implications for medical applications.Cell death discovery · 2026Review
- Mitochondria-derived vesicles with bioenergetic units from brown adipose tissue attenuate cardiac remodeling post-myocardial infarction.Nature communications · 2026Article
- Multivariable genome-wide analysis elucidates the shared genetic architecture, immunosenescence features, and gut-origin therapeutic targets of ulcerative colitis-associated multisystem inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Article
- Microbial Hyaluronidases: From Obscure Virulence Factors to Promising Therapeutic Targets.Biomolecules · 2026Review
- Identification and Validation of MTFP1 as a Mitochondrial Target Restoring Dynamics and ECM Remodeling in Acute Myocardial Infarction.Current issues in molecular biology · 2026Article
- Transcriptomic Analysis of the Amygdala in Subjects with Schizophrenia, Bipolar Disorder and Major Depressive Disorder Reveals Differentially Altered Metabolic Pathways.Schizophrenia bulletin · 2026Article
213 more citing papers are in PubMed but not listed here.
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7 authors.
Funding
Abstract
Inflammation resolution is important for scar formation following myocardial infarction (MI) and requires the coordinated actions of macrophages and fibroblasts. In this study, we hypothesized that exogenous interleukin-10 (IL-10), an anti-inflammatory cytokine, promotes post-MI repair through actions on these cardiac cell types. To test this hypothesis, C57BL/6J mice (male, 3- to 6-month old, n = 24/group) were treated with saline or IL-10 (50 μg/kg/day) by osmotic mini-pump infusion starting at day (d) 1 post-MI and sacrificed at d7 post-MI. IL-10 infusion doubled plasma IL-10 concentrations by d7 post-MI. Despite similar infarct areas and mortality rates, IL-10 treatment significantly decreased LV dilation (1.6-fold for end-systolic volume and 1.4-fold for end-diastolic volume) and improved ejection fraction 1.8-fold (both p < 0.05). IL-10 treatment attenuated inflammation at d7 post-MI, evidenced by decreased numbers of Mac-3-positive macrophages in the infarct (p < 0.05). LV macrophages isolated from d7 post-MI mice treated with IL-10 showed significantly elevated gene expression of M2 markers (Arg1, Ym1, and Tgfb1; all p < 0.05). We further performed RNA-seq analysis on post-MI cardiac macrophages and identified 410 significantly different genes (155 increased, 225 decreased by IL-10 treatment). By functional network analysis grouping, the majority of genes (133 out of 410) were part of the cellular assembly and repair functional group. Of these, hyaluronidase 3 (Hyal3) was the most important feature identified by p value. IL-10 treatment decreased Hyal3 by 28%, which reduced hyaluronan degradation and limited collagen deposition (all p < 0.05). In addition, in vivo IL-10 treatment increased fibroblast activation (proliferation, migration, and collagen production), an effect that was both directly and indirectly influenced by macrophage M2 polarization. Combined, our results indicate that in vivo infusion of IL-10 post-MI improves the LV microenvironment to dampen inflammation and facilitate cardiac wound healing.
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