RAYNAUD PHENOMENON, SCLERODERMA, OVERLAP SYNDROMES AND OTHER FIBROSING SYNDROMES: Edited by Daniel E. Furst and Philip ClementsWhat does global gene expression profiling tell us about the pathogenesis of systemic sclerosis?Assassi, Shervin; Mayes, Maureen D. Author Information University of Texas Health Science Center at Houston, Houston, Texas, USA Correspondence to Shervin Assasi, MD, MS, University of Texas Health Science Center at Houston, 6431 Fannin, MSB 5.266, Houston, TX 77030, USA. Tel: +1 713 500 6905; e-mail: [email protected] Current Opinion in Rheumatology: November 2013 - Volume 25 - Issue 6 - p 686-691 doi: 10.1097/01.bor.0000434672.77891.41 Buy Metrics Abstract Purpose of review The purpose of this study is to review recent hypothesis-driven studies that utilize global gene expression data for elucidating the molecular basis of systemic sclerosis (SSc) and its various clinical manifestations. Recent findings The longitudinal skin gene expression studies indicate that the previously identified molecular subsets are stable over time and might identify inherent subgroups of SSc patients. Skin transcript follow-up studies indicate that the Wnt/β-catenin pathway plays an important role in promotion of fibrogenesis in fibroblasts and preadipocytes. Furthermore, the transcript profile of sclerodermatous graft-versus-host disease (sclGVHD) mice resembles the skin transcriptomes of a subgroup of SSc patientswith IL13/IL4-inducible skin signature wherein the profibrotic chemokine CCL2 plays a key role. The comparison of skin biopsies from SSc patients to skin lesions of patients with cutaneous lupus and dermatomyositis has provided valuable information about the interferon (IFN) signature in these autoimmune diseases. Furthermore, plasma IFN-inducible chemokines correlate with the IFN gene expression score in SSc patients, enabling researchers to examine this molecular signature in large SSc cohorts with serum or plasma collection. Summary Global gene expression profiling in skin and peripheral blood can contribute to a better understanding of SSc pathogenesis and identify novel biomarkers and therapeutic targets. © 2013 Lippincott Williams & Wilkins, Inc.