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

Bindiya Patel, Shyam S. Bansal, Mohamed Ameen Ismahil, Tariq Hamid, Gregg Rokosh, Matthias Mack, Sumanth D. Prabhu

Research output: Contribution to journalArticlepeer-review

179 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)230-244
Number of pages15
JournalJACC: Basic to Translational Science
Volume3
Issue number2
DOIs
StatePublished - Apr 2018

Keywords

  • T cells
  • cardiac remodeling
  • heart failure
  • inflammation
  • macrophages

Fingerprint

Dive into the research topics of 'CCR2+ Monocyte-Derived Infiltrating Macrophages Are Required for Adverse Cardiac Remodeling During Pressure Overload'. Together they form a unique fingerprint.

Cite this