ArticleCirculation2013
Monocyte-directed RNAi targeting CCR2 improves infarct healing in atherosclerosis-prone mice.
Article in Circulation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers, 3 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
173 citing papers in PubMed, 3 syntheses or guidelines pooled it, 25 citations in OpenAlex.
- Nanoparticle-Based Therapies for Myocardial Injury and Heart Failure: A Systematic Review and Translational Appraisal of Preclinical Evidence.Biomolecules · 2026Pooled it
- Monocytes as a convergent nanoparticle therapeutic target for cardiovascular diseases.Advanced drug delivery reviews · 2022Pooled it
- Cardiac repair after myocardial infarction: A two-sided role of inflammation-mediated.Frontiers in cardiovascular medicine · 2022Pooled it
- Cytomegalovirus Latency Fuels Inflammation Following Myocardial Infarction.Circulation research · 2026Article
- Tissue-Resident Macrophages: Linking Physiology and Inflammation in Infection.Clinical reviews in allergy & immunology · 2026Review
- Spatiotemporal Nanotherapy After Myocardial Infarction: Targeting the Inflammatory-to-reparative Transition With Extracellular Vesicles and Engineered Nanoparticles.Cardiovascular drugs and therapy · 2026Review
- Fate-mapping infiltrating monocytes following experimental myocardial infarction reveals differentiation trajectories in the infarcted heart.The Journal of clinical investigation · 2026Article
- Good cop, bad cop? Rethinking the roles of cardiac macrophages in injury.The Journal of clinical investigation · 2026Article
- Preemptive cardioprotection with a small molecule in rodents that suppresses genes predictive of heart failure.Science advances · 2026Article
- Targeting cardiac resident CCR2+ macrophage-secreted MCP-1 to attenuate inflammation after myocardial infarction.Acta biomaterialia · 2026Article
- Pulsed electromagnetic fields treatment ameliorates cardiac function after myocardial infarction in mice and pigs.Journal of advanced research · 2026Article
- Beyond perfusion: a review of peptide radiopharmaceuticals for cardiovascular imaging.Npj imaging · 2025Review
- The spatial and temporal activation of macrophages during fibrosis.Nature reviews. Immunology · 2025Review
- Nanoparticle Drug Delivery Systems for Atherosclerosis: Precision Targeting, Inflammatory Modulation, and Plaque Stabilization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Splenic modulation of the early inflammatory response to regional and global ischemia/reperfusion injury in swine.American journal of physiology. Heart and circulatory physiology · 2025Article
- Immune cell dynamics in heart failure: implicated mechanisms and therapeutic targets.ESC heart failure · 2025Review
- Interventional real-time molecular MRI for targeting early myocardial injury in a pig model.Npj imaging · 2025Article
- The Emergence of Nanotechnology in the Prognosis and Treatment of Myocardial Infarctions.Recent patents on nanotechnology · 2025Review
- Antagonizing CCR2 With Propagermanium Leads to Altered Distribution of Macrophage Subsets and Favorable Tissue Remodeling After Myocardial Infarction in Mice.Cardiovascular therapeutics · 2025Article
- A Synthetic Nanoparticle to Mimic High-Density Lipoprotein for Reverse Cholesterol Transport.Methods in molecular biology (Clifton, N.J.) · 2025Article
113 more citing papers are in PubMed but not listed here.
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Authors and funding
21 authors at 6 institutions in 2 countries.
Funding
Abstract
backgroundExaggerated and prolonged inflammation after myocardial infarction (MI) accelerates left ventricular remodeling. Inflammatory pathways may present a therapeutic target to prevent post-MI heart failure. However, the appropriate magnitude and timing of interventions are largely unknown, in part because noninvasive monitoring tools are lacking. Here, we used nanoparticle-facilitated silencing of CCR2, the chemokine receptor that governs inflammatory Ly-6C(high) monocyte subset traffic, to reduce infarct inflammation in apolipoprotein E-deficient (apoE(-/-)) mice after MI. We used dual-target positron emission tomography/magnetic resonance imaging of transglutaminase factor XIII (FXIII) and myeloperoxidase (MPO) activity to monitor how monocyte subset-targeted RNAi altered infarct inflammation and healing. METHODS AND
resultsFlow cytometry, gene expression analysis, and histology revealed reduced monocyte numbers and enhanced resolution of inflammation in infarcted hearts of apoE(-/-) mice that were treated with nanoparticle-encapsulated siRNA. To follow extracellular matrix cross-linking noninvasively, we developed a fluorine-18-labeled positron emission tomography agent ((18)F-FXIII). Recruitment of MPO-rich inflammatory leukocytes was imaged with a molecular magnetic resonance imaging sensor of MPO activity (MPO-Gd). Positron emission tomography/magnetic resonance imaging detected anti-inflammatory effects of intravenous nanoparticle-facilitated siRNA therapy (75% decrease of MPO-Gd signal; P<0.05), whereas (18)F-FXIII positron emission tomography reflected unimpeded matrix cross-linking in the infarct. Silencing of CCR2 during the first week after MI improved ejection fraction on day 21 after MI from 29% to 35% (P<0.05).
conclusionCCR2-targeted RNAi reduced recruitment of Ly-6C(high) monocytes, attenuated infarct inflammation, and curbed post-MI left ventricular remodeling.
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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.