STAT1 and STAT3 as intracellular regulators of vascular remodeling

被引:39
|
作者
Wincewicz, Andrzej
Sulkowska, Mariola
Rutkowski, Ryszard
Sulkowski, Stanislaw
Musiatowicz, Boguslaw
Hirnle, Tomasz
Famulski, Waldemar
Koda, Mariusz
Sokol, Grzegorz
Szarejko, Przemyslaw
机构
[1] Med Univ Bialystok, Coll Pathol, Dept Pathol, PL-15269 Bialystok, Poland
[2] Med Univ Bialystok, Dr Ludwik Zamenhof Memorial Children Clin Hosp, Dept Pediat Allergol, PL-15274 Bialystok, Poland
[3] Med Univ Bialystok, Publ Clin Hosp, Dept Cardiac Surg, PL-15276 Bialystok, Poland
[4] Frederick Chopin Memorial Voivodeship Specialist, Traumathol Unit, Rzeszow, Poland
[5] Med Univ Bialystok, Dept Family Med & Commun Nursing, PL-15054 Bialystok, Poland
关键词
signal transduction; remodeling; atherosclerosis; statins; apoptosis;
D O I
10.1016/j.ejim.2006.12.007
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The roles of signal transducers and activators of transcription (STAT) proteins are widely discussed in the pathogenesis of cardiovascular diseases. It is highly probable that STAT1 and STAT3 are activated during proliferation and inflammation inside atheromatous plaques. Luminal surfaces of endothelium become thrombogenic because of STAT1-dependent induction of MHC II and STAT3-regulated recruitment of phospholipase A2. As with STAT1, STAT3 seems to mediate stimulation of vascular wall cells by VEGF, HGF, and Ang II. STAT3 can contribute to counteracting apoptosis by eventual cooperation with c-fos and the bcl-xl gene. As pharmacological agents called statins are reported to regulate activities of STAT proteins, these signal messenger proteins could serve as targets for anti-atherogenic therapy. We attempted to review the role of STAT1 and STAT3 proteins in vascular remodeling. (c) 2007 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:267 / 271
页数:5
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