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JACC Basic Transl Sci. 2018 Mar 14;3(2):230-244. doi: 10.1016/j.jacbts.2017.12.006. eCollection 2018 Apr.

CCR2+ Monocyte-Derived Infiltrating Macrophages Are Required for Adverse Cardiac Remodeling During Pressure Overload.

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Department of Medicine, Division of Cardiovascular Disease and Comprehensive Cardiovascular Center, University of Alabama at Birmingham, Birmingham, Alabama.
Department of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
Medical Service, Birmingham VAMC, Birmingham, Alabama.


Although chronic inflammation is a central feature of heart failure (HF), the immune cell profiles differ with different underlying causes. This suggests that for immunomodulatory therapy in HF to be successful, it needs to be tailored to the specific etiology. Here, the authors demonstrate that monocyte-derived C-C chemokine receptor 2 (CCR2)+ macrophages infiltrate the heart early during pressure overload in mice, and that blocking this response either pharmacologically or with antibody-mediated CCR2+ monocyte depletion alleviates late pathological left ventricular remodeling and dysfunction, T-cell expansion, and cardiac fibrosis. Hence, suppression of CCR2+ monocytes/macrophages may be an important immunomodulatory therapeutic target to ameliorate pressure-overload HF.


APC, antigen presenting cell; BNP, B-type natriuretic peptide; CCL, C-C motif chemokine ligand; CCR2, C-C chemokine receptor 2; DC, dendritic cell; EDTA, ethylenediaminetetraacetic acid; EF, ejection fraction; HF, heart failure; ICAM, intercellular adhesion molecule; IFN, interferon; IL, interleukin; LN, lymph node; LV, left ventricular; MerTK, c-mer proto-oncogene tyrosine kinase; PBS, phosphate-buffered saline; T cells; TAC, transverse aortic constriction; TGF, transforming growth factor; TNF, tumor necrosis factor; VCAM, vascular cell adhesion molecule; cardiac remodeling; heart failure; i.p., intraperitoneally; inflammation; macrophages

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