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oai:repisalud.isciii.es:20.500.12105/152642024-09-27T08:04:10Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Roldán-Montero, Raquel author Pérez-Sáez, Juan M author Cerro-Pardo, Isabel author Oller, Jorge author Martinez-Lopez, Diego author Nunez, Estefania author Maller, Sebastian M author Gutierrez-Muñoz, Carmen author Mendez-Barbero, Nerea author Escola-Gil, Joan C author Michel, Jean-Baptiste author Mittelbrunn, Maria author Vazquez, Jesus author Blanco-Colio, Luis M author Rabinovich, Gabriel A author Martin-Ventura, Jose L author 2022-03-18 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 β-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 mitochondrial proteins. Mechanistically, Gal-1 silencing resulted in increased foam cell formation and mitochondrial 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. Sci Adv. 2022 Mar 18;8(11):eabm7322 http://hdl.handle.net/20.500.12105/15264 35294231 10.1126/sciadv.abm7322 2375-2548 Science advances Galectin-1 prevents pathological vascular remodeling in atherosclerosis and abdominal aortic aneurysm.