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β-羟基丁酸通过AMPK/Nrf2途径抑制内质网应激介导的细胞凋亡减轻动脉粥样硬化钙化

β-Hydroxybutyrate Alleviates Atherosclerotic Calcification by Inhibiting Endoplasmic Reticulum Stress-Mediated Apoptosis via AMPK/Nrf2 Pathway.

作者信息

Chen Yu, You Yiran, Wang Xin, Jin Yufeng, Zeng Yupeng, Pan Zhijun, Li Dan, Ling Wenhua

机构信息

Department of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou 510080, China.

Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Guangzhou 510080, China.

出版信息

Nutrients. 2024 Dec 30;17(1):111. doi: 10.3390/nu17010111.

DOI:10.3390/nu17010111
PMID:39796543
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11722964/
Abstract

BACKGROUND: Atherosclerotic calcification (AC) is a common feature of atherosclerotic cardiovascular disease. β-Hydroxybutyrate (BHB) has been identified as a molecule that influences cardiovascular disease. However, whether BHB can influence AC is still unknown. METHODS AND RESULTS: In this study, ApoE mice, fed a Western diet, were used to examine the effects of BHB on AC. Rat vascular smooth muscle cells (VSMCs) were used to verify the impacts of BHB on AC and to explore the underlying mechanisms. The results show that Western diet-challenged ApoE mice, supplemented with BHB for 24 weeks, exhibited reduced calcified areas, calcium content, and alkaline phosphatase (ALP) activity in the aortas, as well as ameliorated severity of AC. Furthermore, BHB downregulated the expression of glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP), thereby reducing endoplasmic reticulum stress (ERS) and ERS-mediated apoptosis in the aortas of the mice. Consistently, in vitro studies showed that BHB reduced ALP activity and calcium content in VSMCs, and inhibited VSMC calcification. Additionally, BHB suppressed ERS-mediated apoptosis in VSMCs. CONCLUSIONS: In summary, the present results demonstrate that BHB can alleviate atherosclerotic calcification by inhibiting ERS-mediated apoptosis. Therefore, BHB may serve as a viable therapeutic agent for AC.

摘要

背景：动脉粥样硬化钙化（AC）是动脉粥样硬化性心血管疾病的一个常见特征。β-羟基丁酸（BHB）已被确认为一种影响心血管疾病的分子。然而，BHB是否能影响AC仍不清楚。 方法与结果：在本研究中，给喂食西方饮食的载脂蛋白E（ApoE）小鼠补充BHB，以研究其对AC的影响。使用大鼠血管平滑肌细胞（VSMCs）来验证BHB对AC的影响并探索其潜在机制。结果显示，在接受西方饮食的ApoE小鼠中补充BHB 24周后，主动脉中的钙化区域、钙含量和碱性磷酸酶（ALP）活性降低，AC的严重程度得到改善。此外，BHB下调了葡萄糖调节蛋白78（GRP78）和C/EBP同源蛋白（CHOP）的表达，从而减轻了小鼠主动脉中的内质网应激（ERS）及ERS介导的细胞凋亡。同样，体外研究表明，BHB降低了VSMCs中的ALP活性和钙含量，并抑制了VSMCs钙化。此外，BHB抑制了VSMCs中ERS介导的细胞凋亡。 结论：总之，目前的结果表明，BHB可通过抑制ERS介导的细胞凋亡来减轻动脉粥样硬化钙化。因此，BHB可能是一种治疗AC的有效药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fee/11722964/6c4517bc9ef4/nutrients-17-00111-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fee/11722964/8ad207d5c8bb/nutrients-17-00111-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fee/11722964/6c4517bc9ef4/nutrients-17-00111-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fee/11722964/9879fe6c8e40/nutrients-17-00111-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fee/11722964/6e5d644dc9a5/nutrients-17-00111-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fee/11722964/a42c92e48286/nutrients-17-00111-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fee/11722964/b7294ee912b5/nutrients-17-00111-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fee/11722964/64d2501bfb6d/nutrients-17-00111-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fee/11722964/ff8e768a0b10/nutrients-17-00111-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fee/11722964/6c4517bc9ef4/nutrients-17-00111-g008.jpg

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引用本文的文献

[1]
Unraveling the Translational Relevance of β-Hydroxybutyrate as an Intermediate Metabolite and Signaling Molecule.

Int J Mol Sci. 2025-7-30

[2]
Ketone Bodies in Cardiovascular Disease: The Vasculature as a Therapeutic Target.

JACC Basic Transl Sci. 2025-7-17

本文引用的文献

[1]
β-Hydroxybutyrate enhances chondrocyte mitophagy and reduces cartilage degeneration in osteoarthritis via the HCAR2/AMPK/PINK1/Parkin pathway.

Aging Cell. 2024-11

[2]
D-β-Hydroxybutyrate Dehydrogenase Mitigates Diabetes-Induced Atherosclerosis through the Activation of Nrf2.

Thromb Haemost. 2023-10

[3]
Empagliflozin Attenuates Vascular Calcification in Mice with Chronic Kidney Disease by Regulating the NFR2/HO-1 Anti-Inflammatory Pathway through AMPK Activation.

Int J Mol Sci. 2023-6-12

[4]
Molecular Mechanisms of Vascular Health: Insights From Vascular Aging and Calcification.

Arterioscler Thromb Vasc Biol. 2023-1

[5]
Exercise and Metformin Intervention Prevents Lipotoxicity-Induced Hepatocyte Apoptosis by Alleviating Oxidative and ER Stress and Activating the AMPK/Nrf2/HO-1 Signaling Pathway in db/db Mice.

Oxid Med Cell Longev. 2022

[6]
Downregulation of HDAC9 by the ketone metabolite β-hydroxybutyrate suppresses vascular calcification.

J Pathol. 2022-11

[7]
Endoplasmic Reticulum Stress and Pathogenesis of Vascular Calcification.

Front Cardiovasc Med. 2022-6-16

[8]
Programmed cell death in atherosclerosis and vascular calcification.

Cell Death Dis. 2022-5-18

[9]
Association Between Weight Change and Increased Likelihood of Abdominal Aortic Calcification Among Men.

J Endocr Soc. 2022-4-22

[10]
Epigenetic Upregulation of H19 and AMPK Inhibition Concurrently Contribute to S-Adenosylhomocysteine Hydrolase Deficiency-Promoted Atherosclerotic Calcification.

Circ Res. 2022-5-13

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