ArticleAnnals of medicine and surgery (2012)2024
IL-4 attenuates myocardial infarction injury by promoting M2 macrophage polarization.
Article in Annals of medicine and surgery (2012), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Effects of Di(2-ethylhexyl) phthalate (DEHP) and hyperoxia on cardiovascular development in newborn rats.Pediatric research · 2026Article
- Macrophage efferocytosis in cardiovascular disease: mechanisms and therapeutic implications.ImmunoHorizons · 2026Review
- Pro- and Anti-Inflammatory Cytokines' Implication in Right Heart Disease, Arrhythmogenesis, and Atrial Fibrillation.Biomolecules · 2026Review
- Inflammation and the Heart: The Role of Traditional Factors.Cardiology research and practice · 2026Review
- Neuro-immune-vascular-stem cell crosstalk in bone/cartilage regeneration: mechanisms, technological advances, and clinical perspectives.Frontiers in bioengineering and biotechnology · 2026Review
- Desloratadine attenuates renal ischemia-reperfusion injury through activation of the Nrf2-GCL-GSH antioxidant pathway.Current research in pharmacology and drug discovery · 2026Article
- Polarized macrophages modulate cardiac structure and contractility under hypoxia in novel immuno-heart on a chip.APL bioengineering · 2025Article
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Authors and funding
7 authors.
Funding
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Abstract
IL-4, an immunoregulatory cytokine, plays a role in various cellular pathways and is known to regulate M2 macrophage polarization. Numerous studies have suggested that promoting the polarization of macrophages toward the M2 phenotype is beneficial for myocardial infarction (MI) recovery. However, whether IL-4 can achieve therapeutic effects in MI by regulating M2 macrophage polarization remains unclear. In this study, the authors observed that IL-4 increased the proportion of M2 macrophages in the ischemic myocardium compared to the PBS group. Additionally, IL-4 reduced the infiltration of inflammatory cells and the expression of proinflammatory-related proteins, while enhancing the expression of genes associated with tissue repair. Furthermore, IL-4 facilitated the recovery of cardiac function and reduced fibrosis in the post-MI phase. Importantly, when macrophages were depleted, the therapeutic benefits of IL-4 mentioned above were attenuated. These findings provide evidence for the effectiveness of IL-4 in treating MI through the regulation of M2 macrophage polarization, thereby encouraging further development of this therapeutic approach.
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