期刊
SCIENCE ADVANCES
卷 8, 期 11, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciadv.abm7322
关键词
-
资金
- Spanish MINECO [PID2019-106814RB-I00, PGC2018-097019-B-I00]
- CAM (Complemento II-CM) [S2017/BMD-3673]
- Fondo de Investigaciones Sanitarias ISCiii-FEDER [RD09/0076/00101, IPT17/0019]
- FEDER Una manera de hacer Europa
- La Caixa Banking Foundation [HR17-00247]
- Instituto de Salud Carlos III (ISCIII)
- Ministerio de Ciencia, Innovacion y Universidades (MCNU)
- Pro CNIC Foundation
- Severo Ochoa Center of Excellence [SEV-2015-0505]
- Ferioli family
- Ostry family
- Caraballo family
- Santander-UAM
- Agencia Nacional de Promocion de la Investigacion
- Desarrollo Tecnologico y la Innovacion (Argentina) [PICT 2010-870]
- Fundacion Sales
- Fundacion Bunge y Born (Argentina)
Galectin-1 (Gal-1) plays a significant role as a therapeutic target for atherosclerosis and abdominal aortic aneurysm (AAA). Lack of Gal-1 leads to severe atherosclerosis and VSMC phenotypic switch, while treatment with recombinant Gal-1 prevents these effects and alleviates the conditions of atherosclerosis and AAA.
Pathological vascular remodeling is the underlying cause of atherosclerosis and abdominal aortic aneurysm (AAA). Here, we analyzed the role of galectin-1 (Gal-1), a beta-galactoside-binding protein, as a therapeutic target for atherosclerosis and AAA. Mice lacking Gal-1 (Lgals1(-/-)) developed severe atherosclerosis induced by pAAV/D377Y-mPCSK9 adenovirus and displayed higher lipid levels and lower expression of contractile markers of vascular smooth muscle cells (VSMCs) in plaques than wild-type mice. Proteomic analysis of Lgals1(-/-) aortas showed changes in markers of VSMC phenotypic switch and altered composition of mitochondria) proteins. Mechanistically, Gal-1 silencing resulted in increased foam cell formation and mitochondria! dysfunction in VSMCs, while treatment with recombinant Gal-1 (rGal-1) prevented these effects. Furthermore, rGal-1 treatment attenuated atherosclerosis and elastase-induced AAA, leading to higher contractile VSMCs in aortic tissues. Gal-1 expression decreased in human atheroma and AAA compared to control tissue. Thus, Gal-1-driven circuits emerge as potential therapeutic strategies in atherosclerosis and AAA.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据