ArticleScientific reports2016
Abrogation of CC chemokine receptor 9 ameliorates ventricular remodeling in mice after myocardial infarction.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Unbiased assessment of 2-arachidonoylglycerol in cardiovascular inflammation.Scientific reports · 2025Article
- Pleiotropic role of CCR9/CCL25 signaling in adriamycin-induced cardiomyopathy.Journal of advanced research · 2025Article
- Advances in fibroblast-based cardiac reprogramming in the treatment of heart disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Qi Yin San Liang San Decoction Relieves Gefitinib-Induced Diarrhea via the Modulation of Chemokines and Innate Immune Responses.Current topics in medicinal chemistry · 2025Article
- Protein Biomarkers of Ultra-Processed Food Consumption and Risk of Coronary Heart Disease, Chronic Kidney Disease, and All-Cause Mortality.The Journal of nutrition · 2024Article
- Overexpression of zinc-finger protein 418 inhibits pathological cardiac remodelling after acute myocardial infarction.ESC heart failure · 2024Article
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities.Circulation research · 2024Review
- Proteomic profiling identifies novel independent relationships between inflammatory proteins and myocardial infarction.European journal of preventive cardiology · 2023Article
- Targeting neuro-immune systems to achieve cardiac tissue repair following myocardial infarction: A review of therapeutic approaches from in-vivo preclinical to clinical studies.Pharmacology & therapeutics · 2023Review
- Macrophages in myocardial infarction.American journal of physiology. Cell physiology · 2022Review
- Inflammation- and Gut-Homing Macrophages, Engineered toInternational journal of molecular sciences · 2021Article
- CCL25 and CCR9 is a unique pathway that potentiates pannus formation by remodeling RA macrophages into mature osteoclasts.European journal of immunology · 2021Article
- Chemokines in Myocardial Infarction.Journal of cardiovascular translational research · 2021Review
- Abrogation of CC Chemokine Receptor 9 Ameliorates Ventricular Electrical Remodeling in Mice After Myocardial Infarction.Frontiers in cardiovascular medicine · 2021Article
- The Roles of CCR9/CCL25 in Inflammation and Inflammation-Associated Diseases.Frontiers in cell and developmental biology · 2021Review
- Post-ischemic Myocardial Inflammatory Response: A Complex and Dynamic Process Susceptible to Immunomodulatory Therapies.Frontiers in cardiovascular medicine · 2021Review
- Oxaliplatin Treatment Alters Systemic Immune Responses.BioMed research international · 2019Article
- Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities.Pharmacology & therapeutics · 2018Review
- Myeloid receptor CD36 is required for early phagocytosis of myocardial infarcts and induction of Nr4a1-dependent mechanisms of cardiac repair.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CC chemokine receptor 9 (CCR9), which is a unique receptor for CC chemokine ligand (CCL25), is mainly expressed on lymphocytes, dendritic cells (DCs) and monocytes/macrophages. CCR9 mediates the chemotaxis of inflammatory cells and participates in the pathological progression of inflammatory diseases. However, the role of CCR9 in the pathological process of myocardial infarction (MI) remains unexplored; inflammation plays a key role in this process. Here, we used CCR9 knockout mice to determine the functional significance of CCR9 in regulating post-MI cardiac remodeling and its underlying mechanism. MI was induced by surgical ligation of the left anterior descending coronary artery in CCR9 knockout mice and their CCR9+/+ littermates. Our results showed that the CCR9 expression levels were up-regulated in the hearts of the MI mice. Abrogation of CCR9 improved the post-MI survival rate and left ventricular (LV) dysfunction and decreased the infarct size. In addition, the CCR9 knockout mice exhibited attenuated inflammation, apoptosis, structural and electrical remodeling compared with the CCR9+/+ MI mice. Mechanistically, CCR9 mainly regulated the pathological response by interfering with the NF-κB and MAPK signaling pathways. In conclusion, the data reveal that CCR9 serves as a novel modulator of pathological progression following MI through NF-κB and MAPK signaling.
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Registered trials
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