Kate S Smigiel1, William C Parks2. 1. Women's Guild Lung Institute, Departments of Medicine and Biomedical Sciences, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, CA, 90048, USA. 2. Women's Guild Lung Institute, Departments of Medicine and Biomedical Sciences, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, CA, 90048, USA. bill.parks@cshs.org.
Abstract
PURPOSE OF REVIEW: Macrophages are central players in the immune response following tissue injury. These cells perform many functions, and the changing tissue microenvironment during injury shapes macrophage phenotype down a variety of polarized pathways. This review summarizes the current knowledge on the roles of macrophages during different stages of tissue injury, repair, and-if repair is not achieved-fibrosis. RECENT FINDINGS: Macrophages present early in inflammation are functionally distinct from those at later stages. The predominant macrophage phenotype must transition from pro-inflammatory to pro-reparative to facilitate wound healing and scar resolution. If macrophages fail to acquire a tissue-healing phenotype, dysregulated signals can be drivers of disease processes, such as sustained, exuberant inflammation-as occurs in arthropathies-and fibrosis. Comprehensive understanding of the roles of specific macrophage populations at different stages of the repair process will support the development of immune-targeted therapies for diseases such as fibrosis.
PURPOSE OF REVIEW: Macrophages are central players in the immune response following tissue injury. These cells perform many functions, and the changing tissue microenvironment during injury shapes macrophage phenotype down a variety of polarized pathways. This review summarizes the current knowledge on the roles of macrophages during different stages of tissue injury, repair, and-if repair is not achieved-fibrosis. RECENT FINDINGS: Macrophages present early in inflammation are functionally distinct from those at later stages. The predominant macrophage phenotype must transition from pro-inflammatory to pro-reparative to facilitate wound healing and scar resolution. If macrophages fail to acquire a tissue-healing phenotype, dysregulated signals can be drivers of disease processes, such as sustained, exuberant inflammation-as occurs in arthropathies-and fibrosis. Comprehensive understanding of the roles of specific macrophage populations at different stages of the repair process will support the development of immune-targeted therapies for diseases such as fibrosis.
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