Brian Wu1,2, Jason S Rockel1, David Lagares3,4,5, Mohit Kapoor6,7,8. 1. The Arthritis Program, Krembil Research Institute, University Health Network, Toronto, Ontario, Canada. 2. Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada. 3. Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. dlagares@mgh.harvard.edu. 4. Department of Medicine, Division of Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. dlagares@mgh.harvard.edu. 5. Fibrosis Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. dlagares@mgh.harvard.edu. 6. The Arthritis Program, Krembil Research Institute, University Health Network, Toronto, Ontario, Canada. mohit.kapoor@uhnresearch.ca. 7. Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada. mohit.kapoor@uhnresearch.ca. 8. Department of Surgery, University of Toronto, Toronto, Ontario, Canada. mohit.kapoor@uhnresearch.ca.
Abstract
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. 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.
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. 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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