Journal
SEMINARS IN LIVER DISEASE
Volume 30, Issue 3, Pages 245-257Publisher
THIEME MEDICAL PUBL INC
DOI: 10.1055/s-0030-1255354
Keywords
Fibrosis; inflammation; collagen; wound healing; stellate cell; myofibroblasts; interleukin-13; transforming growth factor beta; tumor necrosis factor; interleukin-1; interleukin-17; arginase; Relm-alpha; chitinase
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Funding
- Intramural NIH HHS [ZIA AI000829-12, ZIA AI001019-03] Funding Source: Medline
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Macrophages are found in close proximity with collagen-producing myofibroblasts and indisputably play a key role in fibrosis. They produce profibrotic mediators that directly activate fibroblasts, including transforming growth factor-beta 1 and platelet-derived growth factor, and control extracellular matrix turnover by regulating the balance of various matrix metalloproteinases and tissue inhibitors of matrix metalloproteinases. Macrophages also regulate fibrogenesis by secreting chemokines that recruit fibroblasts and other inflammatory cells. With their potential to act in both a pro- and antifibrotic capacity, as well as their ability to regulate the activation of resident and recruited myofibroblasts, macrophages and the factors they express are integrated into all stages of the fibrotic process. These various, and sometimes opposing, functions may be performed by distinct macrophage subpopulations, the identification of which is a growing focus of fibrosis research. Although collagen-secreting myofibroblasts once were thought of as the master producers of fibrosis, this review will illustrate how macrophages function as the master regulators of fibrosis.
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