Vascular endothelial growth factor - key mediator of angiogenesis and promising therapeutical target in ulcerative colitis

被引:5
|
作者
Mateescu, Radu Bogdan [1 ,2 ]
Bastian, Alexandra Eugenia [3 ,4 ]
Nichita, Luciana [3 ,4 ]
Marinescu, Madalina [2 ]
Rouhani, Farid [2 ]
Voiosu, Andrei Mihai [2 ]
Bengus, Andreea [2 ]
Tudorascu, Diana Rodica [5 ]
Popp, Cristiana Gabriela [4 ]
机构
[1] Carol Davila Univ Med & Pharm, Bucharest, Romania
[2] Colentina Univ Hosp, Dept Gastroenterol, Bucharest, Romania
[3] Carol Davila Univ Med & Pharm, Fac Med Dent, Bucharest, Romania
[4] Colentina Univ Hosp, Dept Pathol, Bucharest, Romania
[5] Univ Med & Pharm Craiova, Dept Internal Med, 2 Petru Rares St, Craiova 200349, Romania
来源
关键词
ulcerative colitis; angiogenesis; VEGF; endoglin; oxidative stress; INFLAMMATORY-BOWEL-DISEASE; VEGF; EXPRESSION; DIAGNOSIS; CELLS; CD105;
D O I
暂无
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Ulcerative colitis (UC) is an inflammatory bowel disease, triggered by an inappropriate immune response of colonic mucosa. Angiogenesis is an important part of inflammatory process, enhancing inflammation in a vicious circle that aggravates mucosal damage and remodeling. The most important pathway for angiogenesis in ulcerative colitis involves vascular endothelial growth factor (VEGF) and endoglin (CD105) and can be used as target for adjuvant therapy in order to improve patients' outcome. We present a retrospective cohort study evaluating mucosal expression of VEGF and CD105 and their correlation with patients' evolution and risk of relapse. In our study, patients with UC have correlated increases of VEGF expression and microvessel density (evaluated with CD105 staining), sustaining the hypothesis that angiogenesis is not just a passive process driven by inflammation, but an active player of mucosal lesions in ulcerative colitis.
引用
收藏
页码:1339 / 1345
页数:7
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