期刊
ANNUAL REVIEW OF PATHOLOGY: MECHANISMS OF DISEASE, VOL 8
卷 8, 期 -, 页码 241-276出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-pathol-020712-163930
关键词
myofibroblast; pericyte; fibrotic disease; fibrocyte
类别
资金
- Intramural NIH HHS [ZIA AI000829-15, ZIA AI001019-06] Funding Source: Medline
- NHLBI NIH HHS [R01 HL067967, HL107181, HL067967, P50 HL107181] Funding Source: Medline
- NIDDK NIH HHS [DK87389, P30 DK017047, DK84077, DK93493, R01 DK084077, RC1 DK087389, R01 DK093493] Funding Source: Medline
Myofibroblasts accumulate in the spaces between organ structures and produce extracellular matrix (ECM) proteins, including collagen I. They are the primary effector cells in tissue remodeling and fibrosis. Previously, leukocyte progenitors termed fibrocytes and myofibroblasts generated from epithelial cells through epithelial-to-mesenchymal transition (EMT) were considered the primary sources of ECM-producing myofibroblasts in injured tissues. However, genetic fate mapping experiments suggest that mesenchyme-derived cells, known as resident fibroblasts, and pericytes are the primary precursors of scarforming myofibroblasts, whereas epithelial cells, endothelial cells, and myeloid leukocytes contribute to fibrogenesis predominantly by producing key fibrogenic cytokines and by promoting cell-to-cell communication. Numerous cytokines derived from T cells, macrophages, and other myeloid cell populations are important drivers of myofibroblast differentiation. Monocyte-derived cell populations are key regulators of the fibrotic process: They act as a brake on the processes driving fibrogenesis, and they dismantle and degrade established fibrosis. We discuss the origins, modes of activation, and fate of myofibroblasts in various important fibrotic diseases and describe how manipulation of macrophage activation could help ameliorate fibrosis.
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