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Camellia oleifera meal peptides alleviates atherosclerosis by regulating lipid metabolism through AMPK/ACC/CPT-1 pathway

ABSTRACT: Background: The potential of Camellia oleifera meal peptides（PP) in the treatment of atherosclerosis and its potential mechanism need to be further clarified. Objective: the aim of this study was to clarify the effect of PP in the treatment of atherosclerosis and its potential mechanism. Methods: After cell modeling, it was used to detect the antioxidant, anti-inflammatory and lipid-lowering effects of PP in vitro. As mouse model was used to evaluate the anti atherosclerotic effect of PP in vivo. The changes of protein and metabolites after the treatment of atherosclerosis by PP were studied by liver proteomics, metabonomics and transcriptomics, and the possible mechanism of its regulation of lipid metabolism was clarified. Results:Using cell inflammation model, oxidative damage model and high-fat model, CCK8 test and qPCR detection showed that PP had antioxidant, anti-inflammatory and lipid-lowering effects. The animal results showed that the lipid deposition in the root of aortic valve and liver tissue was reduced, and the PP had the effect of alleviating atherosclerosis. Metabonomics and proteomics analysis showed that the activities of various enzymes related to lipid metabolism were changed after PP treatment, and the lipid metabolism pathway was changed. Transcriptomics analysis showed that AMPK pathway was changed. The experimental results showed that AMPK regulated lipid oxidation pathway to alleviate atherosclerosis in mice through acetyl CoA carboxylase (ACC) - CPT-1 pathway.

ORGANISM(S): Mus musculus

PROVIDER: GSE312428 | GEO | 2026/03/01

REPOSITORIES: GEO

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Project description:Background and Aims Lipid-lowering therapy is a cornerstone in the treatment of atherosclerotic cardiovascular disease (ASCVD). Although some lipid-lowering drugs have demonstrated positive effects in patients with ASCVD, their effects are limited in those with homozygous familial hypercholesterolemia (HoFH). It is essential to seek new lipid-lowering targets. Yes-associated protein (YAP) may be involved in lipid metabolism in liver; therefore, we investigated the function of hepatocyte YAP in hyperlipidemia and atherosclerosis. Methods Hyperlipidemia models were generated in apoE-/- mice or mice injected with AAV8-D377Y-mPCSK9, which degrades and deletes low density lipoprotein receptor (LDLR), by being fed a high cholesterol diet (HCD) for 12 weeks. We measured the expression level of hepatic YAP in these apoE-/- mice. Next, we created YAPΔHep apoE-/- mice to further determine the role of YAP in hyperlipidemia and atherosclerosis. AML12 cells and mice injected with AAV8-D377Y-mPCSK9 or YAPΔHepapoE-/- mice were used to elucidate its mechanism. Finally, apoE-/- or LDLR-/- mice were used to observe the therapeutic efficacy of AAV8-Alb-shYAP for hyperlipidemia and atherosclerosis. Results HCD-fed apoE-/- mice showed increased levels of YAP in the liver. Further investigation indicated that YAPΔHepapoE-/- mice exhibited lighter hyperlipidemia and atherosclerosis than YAPflox/floxapoE-/- mice fed with HCD. Conversely, hepatocyte-specific overexpression of YAP (5S) deteriorated hyperlipidemia and atherosclerosis in HCD-fed apoE-/- mice. Furthermore, the lipid-lowering effect of YAP deficiency in hepatocytes was independent of LDLR. Hepatocyte-specific overexpression of angiopoietin-like-3 (ANGPTL3) aggravated hyperlipidemia and atherosclerosis in YAPΔHepapoE-/- mice, indicating that ANGPTL3 is responsible for the function of YAP in hyperlipidemia. Mechanistically, YAP upregulated ANGPTL3 via TEAD4 in hepatocytes independent of LDLR. Notably, AAV8-Alb-shYAP lowered lipid levels in apoE-/- or LDLR-/- mice. Conclusion Taken together, our findings revealed a novel role for the YAP-TEAD4-ANGPTL3 axis in lipid metabolism independent of LDLR. Inhibition of hepatocyte YAP may be an effective lipid-lowering strategy for HoFH.

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Camellia oleifera meal peptides alleviates atherosclerosis by regulating lipid metabolism through AMPK/ACC/CPT-1 pathway

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