期刊文献+

JAK/STAT信号通路与组织器官纤维化的相关性研究进展 被引量:3

Research progress in correlation between the JAK / STAT signal pathway and tissue or organ fibrosis
下载PDF
导出
摘要 Janus激酶/信号转导与转录激活子(JAK/STAT)是一条依靠多种细胞因子和生长因子共同介导的信号通路,广泛参与了细胞的增殖、分化、凋亡及免疫调节等病理生理过程。多项研究表明,JAK/STAT信号通路对机体不同的组织及器官如肾脏、肝脏、肺、心脏等的纤维化形成过程具有重要的调控作用。该文就近年JAK/STAT信号通路与机体组织器官纤维化形成的相关性研究作一综述。 The JAK/STAT signal pathway is collectively mediated by a variety of cytokines and growth factors, and is extensively involved in cell proliferation, differentiation, apoptosis, immunoregulation and other pathophysiological processes. Many studies demonstrate that JAK/STAT pathway plays an important role in regulating the fibrosis process of different tissues and organs, such as kidney, liver, lung and heart. This study reviewed the correlation between the JAK/STAT signal transduction pathway and the process of tis- sue and organ fibrosis.
出处 《新医学》 2014年第11期710-713,共4页 Journal of New Medicine
基金 浙江省自然科学基金(Y13H050021)
关键词 JANUS激酶 信号转导与转录激活子 信号通路 纤维化 Janus kinase Signal transducers and actirators of transcription Signaling pathway Fibrosis
  • 相关文献

参考文献3

二级参考文献38

  • 1Tarek E Korah,Sawsan El-Sayed,Maathir K ElShafie,Ghada E Hammoda,Manal A Safan.Significance of serum leptin and adiponectin levels in Egyptian patients with chronic hepatitis C virus associated hepatic steatosis and fibrosis[J].World Journal of Hepatology,2013,5(2):74-81. 被引量:7
  • 2Kazuhiro Takahashi,Soichiro Murata,Kiyoshi Fukunaga,Nobuhiro Ohkohchi.Human platelets inhibit liver fibrosis in severe combined immunodeficiency mice[J].World Journal of Gastroenterology,2013,19(32):5250-5260. 被引量:17
  • 3Dameshek W. Some speculations on the myeloproliferative syndromes[J].Blood,1951.372-5.
  • 4Levine RL,Wadleigh M,Cools J. Activating mutation in the tyrosine kinase JAK2 in polycythemia vera,essential thrombocythemia,and myeloid metaplasia with myelofibrosis[J].Cancer Cell,2005,(4):387-97.doi:10.1016/j.ccr.2005.03.023.
  • 5Jones AV,Kreil S,Zoi K. Widespread occurrence of the JAK2 V617F mutation in chronic myeloproliferative disorders[J].Blood,2005.2162-8.doi:10.1182/blood-2005-03-1320.
  • 6James C,Ugo V,Le Couédic JP. A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera[J].Nature,2005.1144-8.doi:10.1038/nature03546.
  • 7Baxter E J,Scott LM,Campbell PJ. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders[J].The Lancet,2005.1054-61.
  • 8Kralovics R,Passamonti F,Buser AS. A gain-of-function mutation of JAK2 in myeloproliferative disorders[J].New England Journal of Medicine,2005.1779-90.doi:10.1056/NEJMoa051113.
  • 9Levine RL,Belisle C,Wadleigh M. X-inactivation-based clonality analysis and quantitative JAK2V617F assessment reveal a strong association between clonality and JAK2V617F in PV but not ET/MMM,and identifies a subset of JAK2V617F-negative ET and MMM patients with clonal hematopoiesis[J].Blood,2006.4139-41.
  • 10Lippert E,Boissinot M,Kralovics R. The JAK2-V617F mutation is frequently present at diagnosis in patients with essential thrombocythemia and polycythemia vera[J].Blood,2006.1865-7.

共引文献95

同被引文献30

  • 1吕晓蕾,赵培,张振刚.心肌纤维化:一个慢性炎症反应过程(英文)[J].中国组织工程研究与临床康复,2007,11(51):10416-10420. 被引量:9
  • 2罗佳,章敬成,刘繁荣,吴冬梅,廖首生,杨宇晴.肝癌组织中FMNL-2和MMP-2的表达及临床病理分析[J].肿瘤防治研究,2014,41(5):460-463. 被引量:6
  • 3Mair M, Blaas L, Osterreicher CH, et al. JAK-STAT signaling in he-parle fibrosis[J]. Front Biosci(Landmark Ed), 2011 ,(16) :2794-2811.
  • 4Vera J, Rateitschak K, Lange F, et al. Systems biology of JAK- STAT signaling in human malignancies[J]. Prog Biophys Mol Bi- ol, 2011,106(2) :426-434.
  • 5Matsui F, Meldrum KK. The role of the Janus kinase family/signal transducer and activator of transcription signaling pathway in fibrot- ic renal disease[ J ]. J Surg Res, 2012,178 (1) :339-345.
  • 6Jatiani SS, Baker SJ, Silverman LR, et al. JAK/STAT pathways in cytokine signaling and myeloproliferative disorders: approaches for targeted therapies [ J ]. Genes Cancer, 2010,1 ( 10 ) :979-993.
  • 7Numasaki M, Watanabe M, Suzuki T, et al. IL-17 enhances the net angiogenic activity and in vivo growth of human non-small cell lung cancer in SCID mice through promoting CXCR-2-dependent angiogenesis[ J]. J Immunol, 2005,175 (9) :617745189.
  • 8Pang M, Kothapally J, Mao H, et al. Inhibition of histone deacety- lase activity attenuates renal fibroblast activation and interstitial fi- brosis in obstructive nephropathy[J]. Am J Physiol Renal Physiol, 2009,297(4) : 1;996-F1005.
  • 9Martfnez-Caselles A, Pons-Minano JA, Vargas-Acosta A, et al. Hepatoportal sclerosis clinical different evolutionary stages: pres- entation of 3 cases and literature review [ J ]. Rev Esp Enferm Dig, 2012,104(2) :94-97.
  • 10Pang M, Ma L, Gong R, et al. A novel STAT3 inhibitor, S31-201, at- tenuates renal interstitial fibroblast activation and interstitial fibrosis in obstructive nephropathy[J]. Kidney Int, 2010,78(3) :257-268.

引证文献3

二级引证文献16

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部