Wincewicz Andrzej, Sulkowska Mariola, Rutkowski Ryszard, Sulkowski Stanislaw, Musiatowicz Boguslaw, Hirnle Tomasz, Famulski Waldemar, Koda Mariusz, Sokol Grzegorz, Szarejko Przemyslaw
Department of Pathology, Waszyngtona St 13, 15-269 Białystok, Collegium Pathologicum, Medical University of Bialystok, Poland.
Eur J Intern Med. 2007 Jul;18(4):267-71. doi: 10.1016/j.ejim.2006.12.007. Epub 2007 May 23.
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.
