Downregulation of CFIm25 amplifies dermal fibrosis through alternative polyadenylation

Tingting Weng, Jing-Jing Huang, E. Wagner, Junsuk Ko, Minghua Wu, N. Wareing, Yu Xiang, Ning-yuan Chen, Ping Ji, Jose G. Molina, K. Volcik, Leng Han, M. Mayes, M. Blackburn, S. Assassi
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引用次数: 21

Abstract

This study implicates the key regulator of alternative polyadenylation, CFIm25 in dermal fibrosis and in systemic sclerosis (scleroderma) pathogenesis. CFIm25 downregulation promotes the expression of profibrotic factors, exaggerates bleomycin-induced skin fibrosis, while CFIm25 restoration attenuates skin fibrosis.
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CFIm25的下调通过选择性聚腺苷化放大皮肤纤维化
该研究揭示了真皮纤维化和系统性硬皮病发病机制中选择性聚腺苷酸化的关键调节因子CFIm25。CFIm25下调可促进促纤维化因子的表达,加重博来霉素诱导的皮肤纤维化,而CFIm25修复可减轻皮肤纤维化。
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