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10.1038/s41598-017-11233-w

http://scihub22266oqcxt.onion/10.1038/s41598-017-11233-w
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C5591217!5591217!28887478
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suck abstract from ncbi


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pmid28887478      Sci+Rep 2017 ; 7 (ä): ä
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  • Stat3 as a potential therapeutic target for rheumatoid arthritis #MMPMID28887478
  • Oike T; Sato Y; Kobayashi T; Miyamoto K; Nakamura S; Kaneko Y; Kobayashi S; Harato K; Saya H; Matsumoto M; Nakamura M; Niki Y; Miyamoto T
  • Sci Rep 2017[]; 7 (ä): ä PMID28887478show ga
  • Rheumatoid arthritis (RA) is a multi-factorial disease characterized by chronic inflammation and destruction of multiple joints. To date, various biologic treatments for RA such as anti-tumor necrosis factor alpha antibodies have been developed; however, mechanisms underlying RA development remain unclear and targeted therapy for this condition has not been established. Here, we provide evidence that signal transducer and activator of transcription 3 (Stat3) promotes inflammation and joint erosion in a mouse model of arthritis. Stat3 global KO mice show early embryonic lethality; thus, we generated viable Stat3 conditional knockout adult mice and found that they were significantly resistant to collagen-induced arthritis (CIA), the most common RA model, compared with controls. We then used an in vitro culture system to screen ninety-six existing drugs to select Stat3 inhibitors and selected five candidate inhibitors. Among them, three significantly inhibited development of arthritis and joint erosion in CIA wild-type mice. These findings suggest that Stat3 inhibitors may serve as promising drugs for RA therapy.
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