Animal study demonstrates that neuraminidase-driven LDL desialylation accelerates aortic lesion formation in ApoE-knockout mice, suggesting glycan removal directly drives atherogenicity.
Atherosclerosis research lacks in vivo models that specifically capture how structural modifications of low-density lipoprotein (LDL) drive disease progression.Our study addresses this unmet need by establishing a reproducible model of chronic LDL desialylation, a glycan-removal process suspected to enhance lipoprotein atherogenicity.We show that neuraminidase-induced LDL modification increases macrophage cholesterol loading and accelerates aortic lesion development even without severe hyperlipidemia.These findings reveal LDL glycosylation status as an independent determinant of atherogenicity and suggest that targeting sialylation pathways may offer new mechanistic and therapeutic insights for cardiovascular disease.
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Kashirskikh et al. (2026) studied this question.
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