ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
The Role of MCPIP1 in Macrophage Polarization and Cardiac Function Post-Myocardial Infarction.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Targeting the ENO1 metabolic checkpoint via microenvironment-responsive nanotherapeutics promotes postinfarction cardiac repair.Science advances · 2026Article
- Cuproptosis and ferroptosis: signal pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Atherosclerotic Cell Fates: A Single-Cell View of ER Stress.Journal of cardiovascular development and disease · 2026Review
- SAMHD1 promotes cardiac repair post myocardial infarction by targeting NR4a1 to regulate macrophage metabolic reprogramming.Journal of advanced research · 2026Article
- Natural polysaccharide-nucleic acid nanocomplex alleviates myocardial infarction by driving chronologically programmed macrophage polarization.Materials today. Bio · 2026Article
- M1 macrophage-derived migrasomes exacerbate post-myocardial infarction injury via guanylate binding protein 5.Journal of nanobiotechnology · 2026Article
- Endogenous and exogenous stimuli-driven intelligent nanocarriers: emerging strategies for the treatment of myocardial infarction.Journal of nanobiotechnology · 2026Review
- Therapeutic Potential of the Deubiquitinase BRCC3 in Attenuating Ischemic Myocardial Injury and Ventricular Remodeling.Research (Washington, D.C.) · 2026Article
- Targeting the heart-immune axis after myocardial infarction: from inflammation to immunomodulation.Frontiers in cardiovascular medicine · 2026Review
- Ferroptosis in the pathogenesis of diabetic cardiomyopathy: mechanisms and therapeutic potential.Cardiovascular diabetology · 2025Review
- The Role of MCPIP1 in Macrophage Polarization and Cardiac Function Post-Myocardial Infarction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Network pharmacological analysis, Mendelian randomization analysis and animal experimental reveal the mechanism of Wenxin Granules in inhibiting heart failure after myocardial infarction: apoptosis and inflammation.Frontiers in cardiovascular medicine · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Macrophages play a critical role in both initiating and resolving inflammation following MI (myocardial infarction). Their polarization is essential for maintaining cardiac function. This study aims to explore the role of MCPIP1(Monocyte chemotactic protein-induced protein 1) in regulating macrophage polarization and its impact on heart-spleen interactions during MI recovery. The role of MCPIP1 was investigated using histological staining, RNA sequencing of bone marrow-derived macrophages, co-culture experiments, and validated by western blot. Compared to controls, myeloid MCPIP1-deficient mice had lower survival rates, larger infarction areas, and more severe inflammatory responses after MI. This was due to increased M1 polarization and impaired conversion to the M2 phenotype. Ferroptosis activation in MCPIP1-deficient macrophages was inhibited by Fer-1 and PFT-α, which promoted M2 polarization and fibroblast activation into myofibroblasts. MCPIP1-deficient MI mice also showed splenomegaly and elevated levels of circulating macrophages, indicating excessive extramedullary hematopoiesis. Splenectomy improved survival rates and reduced infarction size in MCPIP1-deficient mice. MCPIP1 suppresses the P53/ferroptosis pathway to regulate macrophage polarization and TGF-β/SMAD3-mediated fibroblast activation. Its deficiency exacerbates inflammation through abnormal splenic macrophage output, impairing cardiac repair. MCPIP1 is a promising therapeutic target for modulating ferroptosis and heart-spleen communication to protect cardiac function following MI.
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