国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2009年
4期
244-247
,共4页
转化生长因子β%Smad%血管生成%肺纤维化%信号传导
轉化生長因子β%Smad%血管生成%肺纖維化%信號傳導
전화생장인자β%Smad%혈관생성%폐섬유화%신호전도
Transforming growth factor-β Smad%Angiogenesis%Pulmonary fibrosis%Signal transduction
转化生长因子β(transforming growth factor-β,TGF-β)是一种多功能的细胞因子,具有广泛的生物学活性.激活素受体样激酶(activin receptor-like kinase,ALK)是TGF-β的Ⅰ型受体,与其配体结合传导信号.Smad是TGF-β的胞浆递质,参与TGF-β的信号传导.TGF-β超家族信号传导有2条通路:一条是TGF-β/ALK1/Smad1/5途径,与新生血管形成有关;另一条是TGF-β/ALK5/Smad2/3途径,拮抗ALK1信号通道,并与肺纤维化有关.内皮细胞的最终活化状态依赖于2种信号的平衡,可以通过抑制ALK1/Smad1/5途径,使平衡向ALK5/Smad2/3途径移动,从而抑制新生血管形成,使其向纤维化转变,为肿瘤治疗提供一个新的方向.
轉化生長因子β(transforming growth factor-β,TGF-β)是一種多功能的細胞因子,具有廣汎的生物學活性.激活素受體樣激酶(activin receptor-like kinase,ALK)是TGF-β的Ⅰ型受體,與其配體結閤傳導信號.Smad是TGF-β的胞漿遞質,參與TGF-β的信號傳導.TGF-β超傢族信號傳導有2條通路:一條是TGF-β/ALK1/Smad1/5途徑,與新生血管形成有關;另一條是TGF-β/ALK5/Smad2/3途徑,拮抗ALK1信號通道,併與肺纖維化有關.內皮細胞的最終活化狀態依賴于2種信號的平衡,可以通過抑製ALK1/Smad1/5途徑,使平衡嚮ALK5/Smad2/3途徑移動,從而抑製新生血管形成,使其嚮纖維化轉變,為腫瘤治療提供一箇新的方嚮.
전화생장인자β(transforming growth factor-β,TGF-β)시일충다공능적세포인자,구유엄범적생물학활성.격활소수체양격매(activin receptor-like kinase,ALK)시TGF-β적Ⅰ형수체,여기배체결합전도신호.Smad시TGF-β적포장체질,삼여TGF-β적신호전도.TGF-β초가족신호전도유2조통로:일조시TGF-β/ALK1/Smad1/5도경,여신생혈관형성유관;령일조시TGF-β/ALK5/Smad2/3도경,길항ALK1신호통도,병여폐섬유화유관.내피세포적최종활화상태의뢰우2충신호적평형,가이통과억제ALK1/Smad1/5도경,사평형향ALK5/Smad2/3도경이동,종이억제신생혈관형성,사기향섬유화전변,위종류치료제공일개신적방향.
Transforming growth faetor-β(TGF-β) is a multifunctional cytokine which has extensive biologic activities. Activin receptor-like kinase(ALK) is TGF-β type Ⅰ receptor,transduces signal through binding with its ligand. Smad protein is cytoplasmic transmitter for TGF-β, takes part in TGF-β signal transduction. Signal transduction of TGF-β superfamily has two pathways. One is TGF-β/ALK1/Smad1/5 pathway,relates to neovascularization. The other is TGF-β/ALK5/Smad2/3 pathway,relates to antagonism of ALK1 signal pathway and lung fibrosis. The final activation state of endothelial cell depends on the balance of two distinct pathways. It is possible to make the balance move to ALK5/Smad2/3 pathway through inhibiting ALK1/Smad1/5 pathway, which can inhibit neovascularization, switch to fibrosis possible and provides a new method for tumor therapy.