ArticleActa biomaterialia2026
Targeting cardiac resident CCR2+ macrophage-secreted MCP-1 to attenuate inflammation after myocardial infarction.
Article in Acta biomaterialia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it.
- SIRT3 in post-myocardial infarction macrophage reprogramming: linking mitochondrial fitness to inflammation resolution and repair.Frontiers in immunology · 2026Pooled it
- Timing-dependent anti-inflammatory effects of empagliflozin in monocyte-derived macrophages from post-myocardial infarct patients with type 2 diabetes.Cardiovascular diabetology · 2026Trial
- Sustained estimated VLDL-C exposure is associated with cardiometabolic multimorbidity and foam cell dysfunction: evidence from prospective cohorts andJournal of geriatric cardiology : JGC · 2026Article
- Molecular Basis of Adipose-Cardiac Crosstalk in Cardiovascular Diseases: From Mechanisms to Therapeutic Opportunities.Biomolecules · 2026Review
- Effects of Resveratrol on MCP-1/CCL2-Related Readouts in Preclinical Animal Models: A Systematic Review and Meta-Analysis.Biomedicines · 2026Review
- Insights in ischemia/reperfusion injury and cardioprotection: neglected and emerging pathways and therapeutic targets for a personalized therapy.Basic research in cardiology · 2026Review
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Tenascin CNature communications · 2026Article
- Evolocumab early reduces IL-1β/IL-17A and improves left ventricular function in STEMI: an observational study in the real world.Frontiers in pharmacology · 2026Article
- Mitochondria-targeted nanotechnology in cardiovascular diseases: a review of recent advances.Regenerative biomaterials · 2026Review
- CCR2Frontiers in pharmacology · 2026Article
- Bacteria microenvironment-responsive missile microneedles modulate immunity and penetrate biofilm for diabetic wound therapy.Bioactive materials · 2026Article
- The role of macrophages in cardiac diseases: a review of the origins, functional diversity, and therapeutic potential.Frontiers in immunology · 2026Review
- Cardiac resident macrophages: the emerging role in arrhythmogenesis.Frontiers in immunology · 2026Review
- Unraveling the pleiotropic effects of CCR2-dependent signal transduction in fibrosis development.Theranostics · 2026Review
- Identification and validation of biomarkers associated with cellular senescence and demethylation in acute myocardial infarction.Scientific reports · 2025Article
- Citrullinated and Malondialdehyde-Acetaldehyde-Modified Fibrinogen Activates Macrophages and Promotes Coronary Endothelial Cell Inflammation.Current issues in molecular biology · 2025Article
- Advancements in nanomedicine for modulating ischemic cardiomyopathy therapy.Materials today. Bio · 2025Review
- Targeted delivery of engineered adipose-derived stem cell secretome to promote cardiac repair after myocardial infarction.Journal of controlled release : official journal of the Controlled Release Society · 2025Article
- Liriodendrin alleviates myocardial ischemia‑reperfusion injury via partially attenuating apoptosis, inflammation and mitochondria damage in rats.International journal of molecular medicine · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
After myocardial infarction (MI), cardiac resident CCR2+ macrophages release various cytokines and chemokines, notably monocyte chemoattractant protein-1 (MCP-1). MCP-1 is instrumental in recruiting CCR2+ monocytes to the damaged region. The excessive arrival of these monocytes, which then become macrophages, perpetuates inflammation at the site of injury. This continuous inflammation leads to adverse tissue remodeling and compromises cardiac function over time. We hypothesized that neutralizing the MCP-1 secreted by cardiac resident CCR2+ macrophages can mitigate post-MI inflammation by curtailing the recruitment of monocytes and their differentiation into macrophages. In this work, we developed nanoparticles that target the infarcted heart, specifically accumulating in the damaged area after intravenous (IV) administration, and docking onto CCR2+ macrophages. These nanoparticles were designed to slowly release an MCP-1 binding peptide, HSWRHFHTLGGG (HSW), which neutralizes the upregulated MCP-1. We showed that the HSW reduced monocyte migration, inhibited pro-inflammatory cytokine upregulation, and suppressed myofibroblast differentiation in vitro. After IV delivery, the released HSW significantly decreased monocyte recruitment and pro-inflammatory macrophage density, increased cardiac cell survival, attenuated cardiac fibrosis, and improved cardiac function. Taken together, our findings support the strategy of MCP-1 neutralization at the acute phase of MI as a promising way to alleviate post-MI inflammation. STATEMENT OF SIGNIFICANCE: After a myocardial infarction (MI), CCR2+ macrophages resident in the heart release various cytokines and chemokines, notably monocyte chemoattractant protein-1 (MCP-1). MCP-1 is instrumental in attracting CCR2+ monocytes to the damaged region. The excessive arrival of these monocytes, which then become macrophages, perpetuates inflammation at the site of injury. This continuous inflammation leads to adverse tissue remodeling and compromises cardiac function over time. In this work, we tested the hypothesis that neutralizing the MCP-1 secreted by cardiac CCR2+ macrophages can mitigate post-MI inflammation by curtailing the recruitment of monocytes.
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Registered trials
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