title: Monocyte and macrophage contributions to cardiac remodeling.
abstract: The mammalian heart contains a population of resident macrophages that expands in response to myocardial infarction and hemodynamic stress. This expansion occurs likely through both local macrophage proliferation and monocyte recruitment. Given the role of macrophages in tissue remodeling, their contribution to adaptive processes in the heart is conceivable but currently poorly understood. In this review, we discuss monocyte and macrophage heterogeneity associated with cardiac stress, the cell's potential contribution to the pathogenesis of cardiac fibrosis, and describe different tools to study and characterize these innate immune cells. Finally, we highlight their potential role as therapeutic targets.
authors.affiliation: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA.
authors.forename: Maarten
authors.initials: M
authors.lastname: Hulsmans
authors.affiliation: Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA.
authors.forename: Flora
authors.initials: F
authors.lastname: Sam
authors.affiliation: Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA. Electronic address: mnahrendorf@mgh.harvard.edu.
authors.forename: Matthias
authors.initials: M
authors.lastname: Nahrendorf
mesh_terms: D000818:Animals; D015415:Biomarkers; D002450:Cell Communication; D049109:Cell Proliferation; D005355:Fibrosis; D006801:Humans; D008264:Macrophages / Q000276:immunology* / Q000378:metabolism*; D009000:Monocytes / Q000276:immunology* / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D010641:Phenotype; D015398:Signal Transduction; D057170:Translational Research, Biomedical; D020257:Ventricular Remodeling
chemical_list: D015415:Biomarkers
keywords: Cardiac remodeling; Fibrosis; Hemodynamic stress; Macrophages; Monocytes; Myocardial infarction