Galectin-1 prevents pathological vascular remodeling in atherosclerosis and abdominal aortic aneurysm.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 35294231.
- Also identified by DOI 10.1126/sciadv.abm7322 and PMC identifier 8926342.
- Licence recorded as CC BY-NC.
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Abstract
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 (<i>Lgals1<sup>-/-</sup></i>) 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 <i>Lgals1<sup>-/-</sup></i> 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.
Medical subject headings
- Aortic Aneurysm, Abdominal
- Atherosclerosis