ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2020
CXCR7 suppression modulates macrophage phenotype and function to ameliorate post-myocardial infarction injury.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- GPR132 antagonists alleviate atherosclerosis by suppressing M1 polarization and subsequent VSMCs proliferation and migration as revealed by transcriptomic profiling.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Activation of CXCR7 exerts an inhibitory effect on adipogenesis through regulation of β-arrestin2/Wnt and AKT signalling.Adipocyte · 2025Article
- Immune cell dynamics in heart failure: implicated mechanisms and therapeutic targets.ESC heart failure · 2025Review
- FOS as a biomarker for myocardial infarction treatment with Deng's Yangxin Decoction: a systems biology-based analysis.Frontiers in cardiovascular medicine · 2025Article
- Article
- Macrophage heterogeneity in myocardial infarction: Evolution and implications for diverse therapeutic approaches.iScience · 2024Review
- CXCR7 Agonist TC14012 Improves Angiogenic Function of Endothelial Progenitor Cells via Activating Akt/eNOS Pathway and Promotes Ischemic Angiogenesis in Diabetic Limb Ischemia.Cardiovascular drugs and therapy · 2023Article
- Multiple roles of cardiac macrophages in heart homeostasis and failure.Heart failure reviews · 2022Review
- Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022Review
- Review
- Emerging Roles of the Atypical Chemokine Receptor 3 (ACKR3) in Cardiovascular Diseases.Frontiers in endocrinology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectiveMyocardial infarction (MI) is one of the primary causes leading to heart failure in coronary artery disease. However, the mechanisms of macrophage that dominate pathogenesis of MI remain unclear.
methodsMice were induced with MI and pretreated with adenovirus containing indicated shRNA. Post-MI injuries were evaluated by echocardiography. BMDMs and post-MI LV macrophages were used to assess the significance of CXCR7. Macrophages' migration was examined by chemotaxis assay, Cytokine production, phosphorylation of ERK1/2, p38 MAPK and JNK were measured by ELISA.
resultsCXCR7 in macrophages was up-regulated during M1 polarization and following MI in the murine model, with positive correlation with M1 markers but not M2 markers. Besides, CXCR7 down-regulation abolished macrophage M1 polarization. In addition, CXCR7 but not CXCR3 or CXCR4 controlled SDF-1 and I-TAC-mediated chemotaxis and inflammation in M1-like macrophages post-MI, signaling through activating ERK1/2, whereas p38 MAPK and JNK were not involved. Moreover, silencing CXCR7 ameliorated cardiac dysfunction by attenuating infarct area, LVEF and LVFS post-MI along with reduction of CXCR7 expression and ERK1/2 phosphorylation.
conclusionsOur data demonstrate that CXCR7 suppression inhibits macrophages M1 polarization, chemotaxis and inflammation to ameliorate post-MI injury, providing novel insights and promising therapy approaches in post-MI treatment.
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