期刊
CURRENT RHEUMATOLOGY REPORTS
卷 21, 期 6, 页码 -出版社
SPRINGER
DOI: 10.1007/s11926-019-0825-x
关键词
Ephrins; Eph receptor; Ephrin-B2; Fibrosis
类别
资金
- Arthritis Society (Canada)
- NIH [R01 HL147059-01]
- Start-up Package by Massachusetts General Hospital
- Scleroderma Foundation New Investigator Grant
- cleroderma Research Foundation Investigator Initiated Research Grant
- American Thoracic Society Foundation/Pulmonary Fibrosis Foundation Research Grant
- Boehringer Ingelheim
- Unity Biotechnology
- Indalo Therapeutics
- Canada Research Chairs Progra
- Canadian Institute of Health Research
- Natural Sciences and Engineering Research Council of Canada (NSERC)
- Canadian Foundation for Innovation
- Krembil Foundation
- Stem Cell Network
- Toronto General and Western Hospital Foundation
- Arthritis Program, University Health Network
Purpose of Review Fibrosis is a pathological feature of many human diseases that affect multiple organs. The development of anti-fibrotic therapies has been a difficult endeavor due to the complexity of signaling pathways associated with fibrogenic processes, complicating the identification and modulation of specific targets. Evidence suggests that ephrin ligands and Eph receptors are crucial signaling molecules that contribute to physiological wound repair and the development of tissue fibrosis. Here, we discuss recent advances in the understanding of ephrin and Eph signaling in tissue repair and fibrosis. Recent Findings Ephrin-B2 is implicated in fibrosis of multiple organs. Intercepting its signaling may help counteract fibrosis. Summary Ephrins and Eph receptors are candidate mediators of fibrosis. Ephrin-B2, in particular, promotes fibrogenic processes in multiple organs. Thus, therapeutic strategies targeting Ephrin-B2 signaling could yield new ways to treat organ fibrosis.
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