Key result
Exogenous ganglioside GM1 increases aortic atherosclerotic plaque area despite lowering plasma triglycerides in mice.
Why the study?
Endogenous ganglioside GM1 plays an important role in atherogenesis, but the specific in vivo effects of exogenous GM1 on atherosclerosis remained poorly understood.
Does exogenous ganglioside GM1 reduce or exacerbate atherosclerotic plaque formation in apoE–/– mice fed a high-fat diet?
Does exogenous ganglioside GM1 reduce or exacerbate atherosclerotic plaque formation in apoE–/– mice fed a high-fat diet?
Exogenous ganglioside GM1 significantly exacerbates atherosclerotic plaque formation in high-fat diet-fed apoE–/– mice independently of plasma cholesterol levels, contrasting with the atheroprotective effects of its precursor GM3.
Answers are grounded in this paper and cite their sources.
Exogenous GM1 exacerbates plaque in apoE–/– mice; leaves open GM1 pathways as atherosclerosis targets pending human studies.
Background: Atherosclerotic cardiovascular diseases (ASCVDs) are leading causes of mortality and disability worldwide. Endogenous monosialotetrahexosylganglioside (ganglioside GM1), a major component of cell membrane lipid rafts, plays an important role in atherogenesis. However, the specific in vivo effects of exogenous GM1 on atherosclerosis remain poorly understood. Methods: To investigate these effects, an atherosclerotic model was established using apolipoprotein E-deficient (apoE–/–) mice fed a high-fat diet (HFD) for 12 weeks. The treatment group received intravenous injections of GM1 (7.5 mg/kg) via the tail vein once every 3 days, whereas the apoE–/– HFD group received phosphate-buffered saline (PBS). Disease progression was evaluated by monitoring body and liver weights, measuring systemic lipid levels, and quantifying atherosclerotic plaque areas in the aortic arch, whole aorta, and aortic root. Results: Exogenous GM1 treatment significantly increased atherosclerotic plaque formation in the whole aorta and aortic root compared with the apoE–/– HFD group. This effect occurred without increases in total cholesterol (TCH), low-density lipoprotein-cholesterol (LDL-C), or high-density lipoprotein cholesterol (HDL-C) levels, whereas plasma triglyceride (TG) levels were significantly reduced. Conclusions: Exogenous ganglioside GM1 exacerbated atherosclerosis in apoE–/– mice, contrasting with the previously reported atheroprotective effects of its precursor, monosialodihexosylganglioside (GM3). Although the mechanisms underlying this effect remain unclear, potentially involving direct vascular signalling or alterations in lipid raft composition, these findings support further investigation of the role of GM1 and its metabolic pathways as critical targets for further research in atherosclerosis biology.
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Huang et al. (2026) studied Atherosclerosis (high-fat diet-induced in apoE-deficient mice) (n=21). Exogenous ganglioside GM1 vs. Phosphate-buffered saline (PBS) in apoE–/– mice fed a high-fat diet (plus a normal chow control group) was evaluated on Atherosclerotic plaque area percentage in the whole aorta and aortic root (p=<0.05). Exogenous ganglioside GM1 (7.5 mg/kg) significantly increased atherosclerotic plaque area in the whole aorta and aortic root (p < 0.05) and reduced plasma triglycerides (p < 0.05) in apoE–/– mice.
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