Volume 24, Issue 2 pp. 215-222
Perspective Article

Transforming growth factor beta (TGF-β) isoforms in wound healing and fibrosis

Michael K. Lichtman MD

Corresponding Author

Michael K. Lichtman MD

Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts

Veterans’ Administration, Boston Healthcare System, Division of Dermatology, Boston University School of Medicine, Boston, Massachusetts

Michael K. Lichtman, MD, Assistant Professor of Dermatology and Peter E. Pochi,MD, Junior Chair of Research at Boston University School of Medicine, Boston, MA 02118. Tel: 617-638-5597; Fax: 617-638-5519; Email. [email protected]Search for more papers by this author
Marta Otero-Vinas PhD

Marta Otero-Vinas PhD

Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts

Department of Systems Biology, The Tissue Repair and Regeneration Laboratory, University of Vic—Central University of Catalonia, Vic, Spain

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Vincent Falanga MD, FACP

Vincent Falanga MD, FACP

Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts

Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts

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First published: 24 December 2015
Citations: 475

Abstract

Scar formation, with persistent alteration of the normal tissue structure, is an undesirable and significant result of both wound healing and fibrosing disorders. There are few strategies to prevent or to treat scarring. The transforming growth factor beta (TGF-β) superfamily is an important mediator of tissue repair. Each TGF-β isoform may exert a different effect on wound healing, which may be context-dependent. In particular, TGF-β1 may mediate fibrosis in adults’ wounds, while TGF-β3 may promote scarless healing in the fetus and reduced scarring in adults. Thus, TGF-β3 may offer a scar-reducing therapy for acute and chronic wounds and fibrosing disorders.

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