Inactivation of the transcription factor STAT-4 prevents inflammation-driven fibrosis in animal models of systemic sclerosis
Arthritis & Rheumatism2010Vol. 63(3), pp. 800–809
Citations Over TimeTop 10% of 2010 papers
Jérôme Avouac, Barbara G. Fürnrohr, Michal Tomčík, Katrin Palumbo, Pawel Zerr, Angelika Horn, Clara Dees, Alfiya Akhmetshina, Christian Beyer, Oliver Distler, Georg Schett, Yannick Allanore, Jörg H. W. Distler
Abstract
The results of this study demonstrate that the transcription factor STAT-4 exerts potent profibrotic effects by controlling T cell activation and proliferation and cytokine release. These findings confirm the results of genetics studies on the role of STAT-4 in the development of SSc.
Related Papers
- Role of pro- and anti-inflammatory cytokines during inflammation: experimental and clinical findings.(1998)
- → SPARC Oppositely Regulates Inflammation and Fibrosis in Bleomycin-Induced Lung Damage(2011)77 cited
- → Aggravation of Bleomycin-Induced Pulmonary Inflammation and Fibrosis in Mice Lacking Peroxiredoxin I(2011)37 cited
- → HIP/PAP protects against bleomycin‐induced lung injury and inflammation and subsequent fibrosis in mice(2020)9 cited