医学分子生物学杂志
醫學分子生物學雜誌
의학분자생물학잡지
FOREIGN MEDICAL SCIENCES
2015年
2期
120-124
,共5页
吕红丽(综述)%吴瑜瑜(审阅)
呂紅麗(綜述)%吳瑜瑜(審閱)
려홍려(종술)%오유유(심열)
原发性开角型青光眼%转化生长因子-β%骨形态发生蛋白%Smad7
原髮性開角型青光眼%轉化生長因子-β%骨形態髮生蛋白%Smad7
원발성개각형청광안%전화생장인자-β%골형태발생단백%Smad7
primary open-angle glaucoma%transforming growth factor%bone morphogenetic protein%Smad7
眼压升高是原发性开角型青光眼(primary open-angle glaucoma , POAG)发生和发展最主要的危险因素,是由小梁网途径的房水外流排出系统发生病变、房水流出阻力增加所致。 POAG 患者小梁网结构最显著的改变是小梁网近小管组织的纤维细胞外基质增多。现表明小梁网细胞外基质的数量和质量的变化是由多种信号通路相互作用调控其合成和降解的结果。来源于房水的转化生长因子-β1(transforming growth factor-β1, TGF-β1)和转化生长因子-β2(transforming growth factor-β2, TGF-β2)可局部诱导小梁网细胞表达多种细胞外基质。骨形态发生蛋白-7(bone morphogenetic protein-7, BMP-7)和骨形态发生蛋白-4(bone morphogenetic protein-4, BMP-4)可有效地拮抗 TGF-β诱导的细胞外基质沉积。这种拮抗作用是通过 Smad7介导的。 Smad7是抑制 TGF-β2信号的一个关键分子。
眼壓升高是原髮性開角型青光眼(primary open-angle glaucoma , POAG)髮生和髮展最主要的危險因素,是由小樑網途徑的房水外流排齣繫統髮生病變、房水流齣阻力增加所緻。 POAG 患者小樑網結構最顯著的改變是小樑網近小管組織的纖維細胞外基質增多。現錶明小樑網細胞外基質的數量和質量的變化是由多種信號通路相互作用調控其閤成和降解的結果。來源于房水的轉化生長因子-β1(transforming growth factor-β1, TGF-β1)和轉化生長因子-β2(transforming growth factor-β2, TGF-β2)可跼部誘導小樑網細胞錶達多種細胞外基質。骨形態髮生蛋白-7(bone morphogenetic protein-7, BMP-7)和骨形態髮生蛋白-4(bone morphogenetic protein-4, BMP-4)可有效地拮抗 TGF-β誘導的細胞外基質沉積。這種拮抗作用是通過 Smad7介導的。 Smad7是抑製 TGF-β2信號的一箇關鍵分子。
안압승고시원발성개각형청광안(primary open-angle glaucoma , POAG)발생화발전최주요적위험인소,시유소량망도경적방수외류배출계통발생병변、방수류출조력증가소치。 POAG 환자소량망결구최현저적개변시소량망근소관조직적섬유세포외기질증다。현표명소량망세포외기질적수량화질량적변화시유다충신호통로상호작용조공기합성화강해적결과。래원우방수적전화생장인자-β1(transforming growth factor-β1, TGF-β1)화전화생장인자-β2(transforming growth factor-β2, TGF-β2)가국부유도소량망세포표체다충세포외기질。골형태발생단백-7(bone morphogenetic protein-7, BMP-7)화골형태발생단백-4(bone morphogenetic protein-4, BMP-4)가유효지길항 TGF-β유도적세포외기질침적。저충길항작용시통과 Smad7개도적。 Smad7시억제 TGF-β2신호적일개관건분자。
Elevated intraocular pressure (IOP) is the most critical risk factor for primary open angle glaucoma (POAG) . It results from an abnormally high aqueous humor outflow resistance in the juxtacanalicular region of the trabecular meshwork. A distinct structural change in the trabecular meshwork of patients with POAG is the increase in fibrillar extracellular matrix in the juxtacanalicu-lar region of the trabecular meshwork. Recently, research shows that the quality and quantity of the extracellular matrix in the trabecular meshwork are regulated by several signaling molecules that in-teract with each other to promote the synthesis, degradation, or modification of extracellular matrix. Transforming growth factor-β1 and β2 (TGF-β1 and TGF-β2) which derive from the aqueous humor may locally induce the expression of a variety of extracellular matrix molecules in trabecular mesh-work cells. Bone morphogenetic proteins (BMP) -7 and -4 can effectively antagonize the effects of TGF-β on extracellular matrix deposition. The antagonizing effects of BMP-7 are mediated in trabec-ular meshwork cells through Smad7, which is a key molecule to inhibit TGF-β2 signaling in the tra-becular meshwork.
