ArticleAmerican journal of physiology. Heart and circulatory physiology2011
CC chemokine receptor 5 deletion impairs macrophage activation and induces adverse remodeling following myocardial infarction.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
- Meteorin-like regulates cardiac repair via macrophage modulation following myocardial infarction.Basic research in cardiology · 2026Article
- Genetic deficiency of CCL5 exhibits the phenotypes of HFpEF and aggravates apoptotic cardiomyopathy in HFD-induced diabetic mice.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Mechanism of heart failure after myocardial infarction.The Journal of international medical research · 2023Review
- Macrophages in myocardial infarction.American journal of physiology. Cell physiology · 2022Review
- Faster skin wound healing predicts survival after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2022Article
- Chemokines in Myocardial Infarction.Journal of cardiovascular translational research · 2021Review
- Targeted Injection of a Truncated Form of Tissue Inhibitor of Metalloproteinase 3 Alters Post-Myocardial Infarction Remodeling.The Journal of pharmacology and experimental therapeutics · 2020Article
- Exogenous IL-4 shuts off pro-inflammation in neutrophils while stimulating anti-inflammation in macrophages to induce neutrophil phagocytosis following myocardial infarction.Journal of molecular and cellular cardiology · 2020Article
- New Approaches to Target Inflammation in Heart Failure: Harnessing Insights from Studies of Immune Cell Diversity.Annual review of physiology · 2020Review
- Exogenous CXCL4 infusion inhibits macrophage phagocytosis by limiting CD36 signalling to enhance post-myocardial infarction cardiac dilation and mortality.Cardiovascular research · 2019Article
- Resveratrol improves cardiac function by promoting M2-like polarization of macrophages in mice with myocardial infarction.American journal of translational research · 2019Article
- The Mouse Heart Attack Research Tool 1.0 database.American journal of physiology. Heart and circulatory physiology · 2018Article
- LXR/RXR signaling and neutrophil phenotype following myocardial infarction classify sex differences in remodeling.Basic research in cardiology · 2018Article
- Myocardial infarction remodeling that progresses to heart failure: a signaling misunderstanding.American journal of physiology. Heart and circulatory physiology · 2018Review
- Proteomic analysis of the cardiac extracellular matrix: clinical research applications.Expert review of proteomics · 2018Review
- Cardiac macrophage biology in the steady-state heart, the aging heart, and following myocardial infarction.Translational research : the journal of laboratory and clinical medicine · 2018Review
- Early matrix metalloproteinase-9 inhibition post-myocardial infarction worsens cardiac dysfunction by delaying inflammation resolution.Journal of molecular and cellular cardiology · 2016Article
- The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis.Circulation research · 2016Review
- CD36 Is a Matrix Metalloproteinase-9 Substrate That Stimulates Neutrophil Apoptosis and Removal During Cardiac Remodeling.Circulation. Cardiovascular genetics · 2016Article
- Adapting extracellular matrix proteomics for clinical studies on cardiac remodeling post-myocardial infarction.Clinical proteomics · 2016Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Post-myocardial infarction (MI), chemokine homing of inflammatory cells into the injured left ventricle (LV) regulates ventricular remodeling, in part by stimulating the extracellular matrix response. The CC chemokine receptor 5 (CCR5) is a key chemokine receptor expressed on macrophages, and CCR5 ligands are highly upregulated post-MI. We hypothesized that deletion of CCR5 would attenuate adverse remodeling by decreasing inflammatory cell recruitment. Accordingly, we examined LV function, macrophage recruitment and activation, and collagen content in wild-type (WT, n = 25) and CCR5 null (n = 33) mice at 7 days post-MI. Both groups had similar infarct sizes (44 ± 2% in WT and 42 ± 2% in CCR5 null; P = 0.37). However, the LV remodeling index (end diastolic volume/LV mass) increased to a larger extent in CCR5 null (1.28 ± 0.08 μl/mg for CCR5 null and 1.02 ± 0.06 μl/mg for WT; P < 0.05). Although numbers of infiltrated macrophages were similar in WT and CCR5 null mice, CCR5-deficient macrophages isolated from the infarct zone displayed >50% decrease in gene expression levels of proinflammatory activation markers (interleukin-1β, interleukin-6, and tumor necrosis factor-α), as well as anti-inflammatory activation markers (arginase 1, CD163, mannose receptor, and transforming growth factor-β1) compared with WT (all P < 0.05). Concomitant with the reduced macrophage activation, heat shock protein-47 and collagen type I precursor levels in the infarct region decreased in the CCR5 null (1.2 ± 0.3 units in the CCR5 null and 2.3 ± 0.4 units in the WT; P < 0.05), while collagen fragments increased (88.3 ± 5.9 units in the CCR5 null and 32.7 ± 8.5 units in the WT; P < 0.05). We conclude that CCR5 deletion impairs LV remodeling by hindering macrophage activation, which stimulates an imbalance in collagen metabolism and increases the remodeling index.
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