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汉黄芩素通过KLF11介导的对PPARα-YAP1驱动的糖酵解的抑制以及ABCA1/G1介导的胆固醇流出的增强来减轻动脉粥样硬化。

Wogonin Attenuates Atherosclerosis via KLF11-Mediated Suppression of PPARα-YAP1-Driven Glycolysis and Enhancement of ABCA1/G1-Mediated Cholesterol Efflux.

作者信息

Ma Chuanrui, Hua Yunqing, Yang Shu, Zhao Yun, Zhang Wei, Miao Yaodong, Zhang Jing, Feng Boxuan, Zheng Guobin, Li Lan, Liu Zhihao, Zhang Han, Zhu Mingjun, Gao Xiumei, Fan Guanwei

机构信息

First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin, 300381, China.

State Key Laboratory of Component-Based Chinese Medicine, Tianjin, 301617, China.

出版信息

Adv Sci (Weinh). 2025 Jun;12(23):e2500610. doi: 10.1002/advs.202500610. Epub 2025 May 21.

DOI:10.1002/advs.202500610
PMID:40397286
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12199419/
Abstract

Atherosclerosis, a chronic inflammatory disorder and leading cause of cardiovascular disease, is characterized by macrophage-derived inflammation and foam cell formation. Emerging evidence suggests that metabolic reprogramming of macrophages represents a promising therapeutic approach for atherosclerosis management. In this study, the therapeutic potential of wogonin, a bioactive flavonoid isolated from Scutellaria baicalensis, in modulating macrophage metabolism and attenuating atherogenesis is investigated. Wogonin reduces lesion size and plaque vulnerability, accompanied by a reduction in foam cell formation and inflammation. Mechanistically, wogonin reprogrammes macrophage metabolism from glycolysis to fatty acid oxidation (FAO) by activating the PPARα-CPT1α pathway and acts as a mitochondrial protector by activating PPARα. Wogonin also promotes the KLF11 expression and KLF11 knockout exacerbated atherosclerosis and abolishes the inhibitory effect of wogonin on glycolysis and atherosclerosis. KLF11 forms a transcriptional complex with PPARα and YAP1, serving both as a brake on PPARα-YAP1-mediated glycolysis and a transcriptional activator of ABCA1/G1. Collectively, wogonin reprograms macrophage metabolism from glycolysis to FAO through activation of the PPARα-KLF11-YAP1 pathway, thereby reducing inflammation and foam cell formation, ultimately attenuating atherogenesis.

摘要

动脉粥样硬化是一种慢性炎症性疾病，也是心血管疾病的主要病因，其特征是巨噬细胞衍生的炎症和泡沫细胞形成。新出现的证据表明，巨噬细胞的代谢重编程是一种很有前景的动脉粥样硬化治疗方法。在本研究中，研究了从黄芩中分离出的生物活性黄酮汉黄芩素在调节巨噬细胞代谢和减轻动脉粥样硬化发生方面的治疗潜力。汉黄芩素可减小病变大小和斑块易损性，同时减少泡沫细胞形成和炎症。从机制上讲，汉黄芩素通过激活PPARα-CPT1α途径将巨噬细胞代谢从糖酵解重编程为脂肪酸氧化（FAO），并通过激活PPARα充当线粒体保护剂。汉黄芩素还促进KLF11表达，而KLF11基因敲除会加剧动脉粥样硬化，并消除汉黄芩素对糖酵解和动脉粥样硬化的抑制作用。KLF11与PPARα和YAP1形成转录复合物，既是PPARα-YAP1介导的糖酵解的制动器，也是ABCA1/G1的转录激活剂。总体而言，汉黄芩素通过激活PPARα-KLF11-YAP1途径将巨噬细胞代谢从糖酵解重编程为FAO，从而减少炎症和泡沫细胞形成，最终减轻动脉粥样硬化的发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37f7/12199419/62ba341a95ff/ADVS-12-2500610-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37f7/12199419/901d6ab04b44/ADVS-12-2500610-g010.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37f7/12199419/ac4cfd98cad0/ADVS-12-2500610-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37f7/12199419/62ba341a95ff/ADVS-12-2500610-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37f7/12199419/901d6ab04b44/ADVS-12-2500610-g010.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37f7/12199419/724fa0c01bcb/ADVS-12-2500610-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37f7/12199419/c2e8b0d28b85/ADVS-12-2500610-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37f7/12199419/4efcce48cd45/ADVS-12-2500610-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37f7/12199419/efc79f3b0da2/ADVS-12-2500610-g005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37f7/12199419/62ba341a95ff/ADVS-12-2500610-g009.jpg

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本文引用的文献

1
ECM Microenvironment in Vascular Homeostasis: New Targets for Atherosclerosis.血管内稳态中的 ECM 微环境：动脉粥样硬化的新靶点。
Physiology (Bethesda). 2024 Sep 1;39(5):0. doi: 10.1152/physiol.00028.2023.
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Wogonin alleviates sepsis-induced acute lung injury by modulating macrophage polarization through the SIRT1-FOXO1 pathways.汉黄芩素通过 SIRT1-FOXO1 通路调节巨噬细胞极化缓解脓毒症诱导的急性肺损伤。
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Wogonin inhibits the migration and invasion of fibroblast-like synoviocytes by targeting PI3K/AKT/NF-κB pathway in rheumatoid arthritis.
汉黄芩素通过靶向类风湿关节炎中的PI3K/AKT/NF-κB信号通路抑制成纤维样滑膜细胞的迁移和侵袭。
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Immunometabolism and immune response regulate macrophage function in atherosclerosis.免疫代谢和免疫反应调节动脉粥样硬化中的巨噬细胞功能。
Ageing Res Rev. 2023 Sep;90:101993. doi: 10.1016/j.arr.2023.101993. Epub 2023 Jun 27.
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Author Correction: Wogonin suppresses osteopontin expression in adipocytes by activating PPARα.作者更正：汉黄芩素通过激活过氧化物酶体增殖物激活受体α（PPARα）抑制脂肪细胞中骨桥蛋白的表达。
Acta Pharmacol Sin. 2023 Jun;44(6):1304. doi: 10.1038/s41401-022-01034-x. Epub 2022 Dec 12.
6
Construction of Wogonin Nanoparticle-Containing Strontium-Doped Nanoporous Structure on Titanium Surface to Promote Osteoporosis Fracture Repair.构建载高乌甲素纳米粒子的锶掺杂纳米多孔结构于钛表面以促进骨质疏松性骨折修复。
Adv Healthc Mater. 2022 Nov;11(21):e2201405. doi: 10.1002/adhm.202201405. Epub 2022 Sep 7.
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Suppression of PFKFB3-driven glycolysis restrains endothelial-to-mesenchymal transition and fibrotic response.抑制 PFKFB3 驱动的糖酵解可抑制血管内皮细胞向间充质细胞转化和纤维化反应。
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