ArticleInternational journal of nanomedicine2018
Effect of CCR2 inhibitor-loaded lipid micelles on inflammatory cell migration and cardiac function after myocardial infarction.
Article in International journal of nanomedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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Who cites it
53 citing papers in PubMed, 77 citations in OpenAlex.
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- Phosphatidylserine-Based Liposomes Encapsulating DMX-5804 Protect Against Doxorubicin-Induced Cardiotoxicity.bioRxiv : the preprint server for biology · 2026Article
- Lymphatic Endothelial C-C Motif Chemokine Ligand 2 Enhances Lymphangiogenesis and Lymphatic Clearance of Macrophages Following Myocardial Infarction.Journal of the American Heart Association · 2026Article
- Migration of Cardiac Cells: Hot Topics that have not Attracted Clinical Attention.International journal of medical sciences · 2026Review
- Peptide-functionalized periodic mesoporous silica nanoparticles for monocyte-specific TET3 Silencing enhance cardiac repair after acute myocardial infarction.Journal of nanobiotechnology · 2025Article
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- Immune cell dynamics in heart failure: implicated mechanisms and therapeutic targets.ESC heart failure · 2025Review
- Complex regulation of cardiac fibrosis: insights from immune cells and signaling pathways.Journal of translational medicine · 2025Review
- Pharmacological antagonism of Ccr2+ cell recruitment to facilitate regenerative tendon healing.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025Article
- Heart failure, inflammation and exercise.International journal of biological sciences · 2025Review
- Nanoparticle-based drug delivery systems targeting inflammatory immune mechanisms in acute myocardial infarction: current advances and perspectives.Frontiers in cardiovascular medicine · 2025Review
- Hypoxia sensing in resident cardiac macrophages regulates monocyte fate specification following ischemic heart injury.Nature cardiovascular research · 2024Article
- Pharmacological Antagonism of Ccr2+ Cell Recruitment to Facilitate Regenerative Tendon Healing.bioRxiv : the preprint server for biology · 2024Article
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities.Circulation research · 2024Review
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Macrophage-based therapeutic approaches for cardiovascular diseases.Basic research in cardiology · 2024Review
- Advanced Nanomedicine Approaches for Myocardial Infarction Treatment.International journal of nanomedicine · 2024Review
- Application of Hydrogels in Cardiac Regeneration.Cardiology and therapy · 2023Review
- Research Advances in Targeted Therapy for Heart Failure.Reviews in cardiovascular medicine · 2023Review
- Control of the post-infarct immune microenvironment through biotherapeutic and biomaterial-based approaches.Drug delivery and translational research · 2023Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAfter myocardial infarction (MI), inflammatory cells infiltrate the infarcted heart in response to secreted stimuli. Monocytes are recruited to the infarct via CCR2 chemokine receptors along a CCL2 concentration gradient. While infiltration of injured tissue with monocytes is an important component of the reparatory response, excessive or prolonged inflammation can adversely affect left ventricular remodeling and worsen clinical outcomes. MATERIALS AND
methodsHere, we developed poly(ethylene glycol) (PEG)-distearoylphos-phatidylethanolamine (PEG-DSPE) micelles loaded with a small molecule CCR2 antagonist to inhibit monocyte recruitment to the infarcted myocardium. To specifically target CCR2-expressing cells, PEG-DSPE micelles were further surface decorated with an anti-CCR2 antibody.
resultsTargeted PEG-DSPE micelles showed eight-fold greater binding to CCR2-expressing RAW 264.7 monocytes than plain, non-targeted PEG-DSPE micelles. In a mouse model of MI, CCR2-targeting PEG-DSPE micelles loaded with a CCR2 small molecule antagonist significantly decreased the number of Ly6C
conclusionBoth non-targeted and CCR2-targeting PEG-DSPE micelles showed a trend toward improving cardiac function. As such, PEG-DSPE micelles represent a promising cardiac therapeutic platform.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.