中国药理学通报
中國藥理學通報
중국약이학통보
CHINESE PHARMACOLOGICAL BULLETIN
2015年
2期
170-174,175
,共6页
谷元婧%孙妩弋%张森%吴晶晶%魏伟
穀元婧%孫嫵弋%張森%吳晶晶%魏偉
곡원청%손무익%장삼%오정정%위위
β-arrestins%纤维化疾病%细胞外基质%G蛋白偶联受体%信号转导%受体酪氨酸激酶
β-arrestins%纖維化疾病%細胞外基質%G蛋白偶聯受體%信號轉導%受體酪氨痠激酶
β-arrestins%섬유화질병%세포외기질%G단백우련수체%신호전도%수체락안산격매
β-arrestins%firotic disease%extracellular matrix%G protein coupled receptor%signal transduction%receptor tyrosine ki-nase
β-arrestins是在提纯β-肾上腺素受体激酶(β-adrener-gic receptor kinase,β-ARK)的过程中发现的一类重要的接头蛋白和信号调控蛋白,对绝大部分G蛋白偶联受体( G pro-tein-coupled receptor,GPCR)介导的信号转导都具有调节作用。纤维化疾病如肝纤维化、肺纤维化、心血管纤维化等,其发病因素和临床表现各不相同,但最终的病理特征都是细胞外基质(extracellular matrix,ECM)在组织器官内过度沉积。大量研究表明,β-arrestins 在纤维化疾病的炎症反应、ECM沉积等作用中发挥重要作用,该文就β-arrestins在纤维化疾病中的研究现状和发展前景作一综述。
β-arrestins是在提純β-腎上腺素受體激酶(β-adrener-gic receptor kinase,β-ARK)的過程中髮現的一類重要的接頭蛋白和信號調控蛋白,對絕大部分G蛋白偶聯受體( G pro-tein-coupled receptor,GPCR)介導的信號轉導都具有調節作用。纖維化疾病如肝纖維化、肺纖維化、心血管纖維化等,其髮病因素和臨床錶現各不相同,但最終的病理特徵都是細胞外基質(extracellular matrix,ECM)在組織器官內過度沉積。大量研究錶明,β-arrestins 在纖維化疾病的炎癥反應、ECM沉積等作用中髮揮重要作用,該文就β-arrestins在纖維化疾病中的研究現狀和髮展前景作一綜述。
β-arrestins시재제순β-신상선소수체격매(β-adrener-gic receptor kinase,β-ARK)적과정중발현적일류중요적접두단백화신호조공단백,대절대부분G단백우련수체( G pro-tein-coupled receptor,GPCR)개도적신호전도도구유조절작용。섬유화질병여간섬유화、폐섬유화、심혈관섬유화등,기발병인소화림상표현각불상동,단최종적병리특정도시세포외기질(extracellular matrix,ECM)재조직기관내과도침적。대량연구표명,β-arrestins 재섬유화질병적염증반응、ECM침적등작용중발휘중요작용,해문취β-arrestins재섬유화질병중적연구현상화발전전경작일종술。
β-arrestins, a kind of important adaptor protein and signal transduction protein found in the purification process ofβ-adrenergic receptor kinase (β-ARK) ,were first identified as pro-teins that have the ability to desensitize G protein-coupled recep-tors ( GPCR) . Fibrosis is defined by the overgrowth, hardening, and scarring of various tissues and is attributed to excess deposi-tion of extracellular matrix ( ECM ) components including colla-gen . A large number of studies have shown thatβ-arrestins play an important role in the process of fibrotic diseases, involved in inflammatory response and excess deposition of ECM. This re-view discusses the research status and development prospects ofβ-arrestins-mediated fibrotic diseases.