The role of TGF-beta signaling in the pathogenesis of fibrosis in scleroderma

• Authors: H. Ihn
• Languages of publication: EN

Abstracts

EN

Excessive extracellular matrix (ECM) deposition in the skin, lung, and other organs is a hallmark of systemic sclerosis (SSc). The pathogenesis of SSc is still poorly understood, but increasing evidence suggests that transforming growth factor (TGF)-beta is a key mediator of tissue fibrosis as a consequence of ECM accumulation in pathologic states such as systemic sclerosis. TGF-beta regulates diverse biological activities including cell growth, cell death or apoptosis, cell differentiation, and extracellular matrix (ECM) synthesis. TGF-beta is known to induce the expression of ECM proteins in mesenchymal cells, and to stimulate the production of protease inhibitors that prevent enzymatic breakdown of the ECM. This review focuses on the possible role of TGF-beta in the pathogenesis of fibrosis in SSc.

Keywords

EN

FIBROSIS; SIGNAL TRANSDUCTION; SYSTEMIC SCLEROSIS; TRANSFORMING GROWTH FACTOR

Discipline

• IMMUNOLOGY: IMMUNOLOGY

• Publisher: Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences
• Journal: Archivum Immunologiae et Therapiae Experimentalis
• Year: 2002
• Volume: 50
• Issue: 5
• Pages: 325-332

Contributors

author

H. Ihn

• Document Type: REVIEW
• Publication order reference: H. Ihn, Department of Dermatology, Faculty of Medicine, University of Tokyo, Tokyo, Japan