期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 217, 期 3, 页码 -出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20190103
关键词
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资金
- National Institutes of Health [R01 HL76246, R01 HL85440]
- US Department of Defense [PR151134, PR151029, PR181464]
TGF-beta is extensively implicated in the pathogenesis of fibrosis. In fibrotic lesions, spatially restricted generation of bioactive TGF-beta from latent stores requires the cooperation of proteases, integrins, and specialized extracellular matrix molecules. Although fibroblasts are major targets of TGF-beta, some fibrogenic actions may reflect activation of other cell types, including macrophages, epithelial cells, and vascular cells. TGF-beta-driven fibrosis is mediated through Smad-dependent or non-Smad pathways and is modulated by coreceptors and by interacting networks. This review discusses the role of TGF-beta in fibrosis, highlighting mechanisms of TGF-beta activation and signaling, the cellular targets of TGF-beta actions, and the challenges of therapeutic translation.
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