Amentoflavone attenuates abdominal aortic aneurysm progression by suppressing vascular smooth muscle cell phenotypic switching <italic style="font-style: italic">via</italic> targeting NF-κB-MMP2/9 axis

LIN Xin; XIE Wenwen; DING Wei; YU Junyi; ZENG Chunyu

doi:10.16016/j.2097-0927.202604083

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Amentoflavone attenuates abdominal aortic aneurysm progression by suppressing vascular smooth muscle cell phenotypic switching via targeting NF-κB-MMP2/9 axis

Basic Medicine | 更新时间：2026-05-30

- Amentoflavone attenuates abdominal aortic aneurysm progression by suppressing vascular smooth muscle cell phenotypic switching via targeting NF-κB-MMP2/9 axis
- Journal of Army Medical University Vol. 48, Issue 10, Pages: 1353-1367(2026)
- 作者机构：
  
  陆军军医大学（第三军医大学）大坪医院心内科，重庆
- 作者简介：
  
  YU Junyi， E-mail： yujunyi@tmmu.edu.cn
  ZENG Chunyu， E-mail： zengchunyu@tmmu.edu.cn
- 基金信息：
  
  the General Program of National Natural Science Foundation of China(82470506)
- DOI：10.16016/j.2097-0927.202604083
  CLC： R285.5;R322.12;R543.13
- Received：24 April 2026，
  
  Revised：2026-04-30，
  
  Accepted：02 May 2026，
  
  Published：30 May 2026
- 稿件说明：
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林鑫，谢汶纹，丁伟，等.穗花杉双黄酮通过靶向NF-κB-MMP2/9轴抑制血管平滑肌细胞表型转换减缓腹主动脉瘤进展［J］.陆军军医大学学报，2026，48（10）：1353-1367.DOI：10.16016/j.2097-0927.202604083.

LIN X，XIE W W，DING W，et al.Amentoflavone attenuates abdominal aortic aneurysm progression by suppressing vascular smooth muscle cell phenotypic switching via targeting NF-κB–MMP-2/9 axis［J］.J Army Med Univ，2026，48（10）：1353-1367.DOI：10.16016/j.2097-0927.202604083.
林鑫，谢汶纹，丁伟，等.穗花杉双黄酮通过靶向NF-κB-MMP2/9轴抑制血管平滑肌细胞表型转换减缓腹主动脉瘤进展［J］.陆军军医大学学报，2026，48（10）：1353-1367.DOI：10.16016/j.2097-0927.202604083. DOI：

LIN X，XIE W W，DING W，et al.Amentoflavone attenuates abdominal aortic aneurysm progression by suppressing vascular smooth muscle cell phenotypic switching via targeting NF-κB–MMP-2/9 axis［J］.J Army Med Univ，2026，48（10）：1353-1367.DOI：10.16016/j.2097-0927.202604083. DOI：

摘要

目的

探究穗花杉双黄酮（amentoflavone，AMF）影响腹主动脉瘤（abdominal aortic aneurysm，AAA）发生发展的作用及机制，为其防治提供新的候选药物与理论依据。

方法

①动物实验。以血管紧张素Ⅱ（angiotensin Ⅱ，Ang Ⅱ）诱导构建AAA小鼠模型：将6~8周龄ApoE

-/-

雄性小鼠按随机数字表法分为6组（

=10）：生理盐水+DMSO组（皮下泵入生理盐水）、生理盐水+AMF组、Ang Ⅱ+DMSO组［皮下泵入Ang Ⅱ 1 000 ng/（kg·min）］、Ang Ⅱ+AMF组（AMF浓度为10、20、50 mg/kg）。建模后的第2天腹腔注射AMF（10、20、50 mg/kg）或其溶剂DMSO 100 μL，每2天1次，建模周期为28 d，建模终点根据AAA成瘤率选择最优浓度20 mg/kg用于后续实验。再以弹性蛋白酶外膜孵育诱导构建AAA小鼠模型：将6~8周龄C57BL/6J雄性小鼠按随机数字表法分为4组（

=6）：假手术+DMSO组、假手术+AMF组（主动脉外膜孵育高温失活的弹性蛋白酶20 min）、弹性蛋白酶+DMSO组、弹性蛋白酶+AMF组（主动脉外膜孵育弹性蛋白酶20 min），建模周期为14 d，AMF或DMSO的注射方式和时间同Ang Ⅱ模型。建模期内记录小鼠生存情况；建模终点以血管超声检测腹主动脉扩张程度，采用HE、VVG染色检测腹主动脉弹性纤维的降解程度。RT-qPCR和Western blotting检测基质金属蛋白酶2（matrix metalloproteinase 2，MMP2）和MMP9的表达水平。②网络药理学分析。从Genecards数据库检索、选取标注为与AAA相关的前2 000个基因，构成AAA靶点集合。为预测可能作用于AAA的物质，采用Galaxy WEB、Super-PRED和SwissTargetPrediction这3个在线工具预测AMF的潜在靶点，获得399个AMF相关靶点构成靶点集合。将AAA和AMF靶点集取交集，重叠部分为

共同靶点，输入STRING数据库构建蛋白质-蛋白质相互作用（protein-protein interaction，PPI）网络，将PPI网络数据导入Cytoscape进行网络可视化和图形优化。③细胞实验。提取成年雄性SD大鼠的原代腹主动脉血管平滑肌细胞（rat aortic vascular smooth muscle cell， RAVSMC）行体外培养，用血小板衍生生长因子BB（platelet-derived growth factor BB，PDGFBB）诱导细胞发生表型转换，将细胞随机分为4组（

=4）：DMSO+CTL组、DMSO+PDGFBB组、AMF+CTL组（浓度为20 μmol/L）、AMF+PDGFBB（浓度为25 ng/mL）组。RT-qPCR和Western blotting检测Calponin、αSMA、MMP2、MMP9的表达水平，Western blotting检测NF-κB信号通路分子（IκBα和P-IκBα）的蛋白水平，免疫荧光染色检测p65的入核情况，CCK-8实验检测RAVSMC的增殖水平，划痕实验和Transwell细胞小室实验检测RAVSMC的迁移能力。通路逆转实验，将细胞随机分为4组（

=4）：DMSO+CTL组、DMSO+PDGFBB组、AMF+PDGFBB组（处理同前）、AMF+PDGFBB+TNF-α（浓度为20 ng/mL）组，RT-qPCR和Western blotting检测Calponin、αSMA、MMP2、MMP9的表达水平。

结果

①AMF能显著提高Ang Ⅱ诱导的AAA模型小鼠的生存率（

0.05）、降低AAA的发病率、减小腹主动脉的扩张程度（

0.01）、减弱中膜弹性纤维的断裂降解（

0.001），抑制AAA组织中MMP2（

0.01）、MMP9（

0.05）的表达。AMF能够显著减小弹性蛋白酶诱导的AAA模型小鼠腹主动脉的扩张程度（

0.001），减弱中膜弹性纤维的断裂降解（

0.001），抑制AAA组织中MMP2（

0.001）、MMP9（

0.05）的表达。②网络药理学PPI分析表明，MMP2和MMP9处于治疗靶点网络的核心位置。③RT-qPCR显示AMF（20 μmol/L）处理显著抑制了由PDGFBB（25 ng/mL）诱导的RAVSMC的MMP2（

0.05）、MMP9（

0.01）mRNA水平升高，提高了Calponin（

0.001）、αSMA（

0.05）mRNA水平；Western blotting显示AMF抑制了由PDGFBB诱导的MMP2（

0.001）、MMP9（

0.001）蛋白水平升高，以及Calponin（

0.01）、αSMA（

0.001）蛋白水平的下降；CCK-8实验显示AMF显著抑制了由PDGFBB诱导的细胞过度增殖（

0.001）；划痕实验和Transwell细胞小室实验显示AMF显著抑制了由PDGFBB诱导的细胞迁移能力（

0.001）。TRRUST转录因子网络分析提示RELA（p65）是排名首位的转录因子；Western blotting显示AMF明显降低IκBα的磷酸化水平（

0.001）；免疫荧光染色结果提示AMF处理有效地降低p65的入核水平，从而抑制NF-κB信号通路。通路逆转实验中，RT-qPCR显示TNF-α（20 ng/mL）处理抑制了AMF诱导的MMP2（

=0.087）、MMP9（

0.05）mRNA水平的下降，以及Calponin（

0.05）、αSMA（

0.05）mRNA水

平的上升；Western blotting显示TNF-α抑制了AMF诱导的MMP2（

0.001）、MMP9（

0.001）蛋白水平的下降，以及Calponin（

0.05）、αSMA（

=0.063）蛋白水平的上升。

结论

AMF 通过靶向NF-κB-MMP2/9轴来减缓AAA的发展，体现了其作为防治AAA新型药物的潜力。

Abstract

Objective

To investigate the role and mechanism of amentoflavone (AMF) in abdominal aortic aneurysm (AAA) pathogenesis

providing novel therapeutic candidates and theoretical foundations.

Methods

①Animal studies: AAA models were induced by angiotensin Ⅱ (Ang Ⅱ) in 6 to 8-week-old male ApoE⁻/⁻ mice randomized (

=10/group) into saline+DMSO

saline+AMF

Ang Ⅱ+DMSO (1 000 ng·kg⁻¹·min⁻¹)

and Ang Ⅱ+AMF (10

50 mg/kg) groups. AMF or DMSO (100 μL) was intraperitoneally administered every 48 h from day 2 for 28 d; 20 mg/kg AMF (optimal dose by AAA incidence) was selected for subsequent experiments. Alternatively

AAA was induced by periaortic elastase incubation in C57BL/6J mice randomized (

=6) into sham+DMSO

sham+AMF (heat-inactivated elastase)

elastase+DMSO

and elastase+AMF groups for 14 d with identical AMF/DMSO protocols. Survival was monitored; AAA dilation was assessed by ultrasonography; elastic fiber degradation was evaluated

via

HE and VVG staining; MMP2/MMP9 expression was quantified by RT-qPCR/Western blotting. ②Network pharmacology: AAA-related targets (top 2 000 genes from Genecards) and AMF targets (predicted

via

Galaxy WEB/SuperPred/SwissTargetPrediction) were intersected; protein-protein interaction (PPI) networks were constructed using STRING and visualized in Cytoscape. ③Cellular experiments: Primary rat aortic vascular smooth muscle cells (RAVSMCs) were treated with: DMSO+CTL

DMSO+PDGFBB (25 ng/mL)

AMF+CTL (20 μmol/L)

or AMF+PDGFBB. Calponin

αSMA

MMP2

MMP9

IκBα

and phospho-IκBα levels were assessed; NF-κB activation was ev

aluated

via

p65 nuclear translocation; proliferation (CCK-8) and migration (scratch/Transwell) were measured. Pathway rescue: TNF-α (20 ng/mL) was co-administered with AMF+PDGFBB to assess target reversibility.

Results

① AMF significantly improved the survival rate of Ang Ⅱ-induced AAA model mice (

0.05)

decreased the incidence of AAA

reduced the degree of abdominal aortic dilation (

0.01)

attenuated elastic fiber fragmentation and degradation in the aortic media (

0.001)

and inhibited the expression of MMP2 (

0.01) and MMP9 (

0.05) in AAA tissues. AMF also markedly reduced the extent of abdominal aortic dilation (

0.001)

mitigated medial elastic fiber disruption (

0.001)

and suppressed MMP2 (

0.001) and MMP9 (

0.05) expression in the elastase-induced AAA model.② PPI network analysis revealed that MMP2 and MMP9 occupied a core position within the therapeutic target network.③ RT-qPCR analysis showed that AMF treatment (20 μmol/L) significantly reversed the PDGF BB (25 ng/mL)-induced increases in MMP2 (

0.05) and MMP9 (

0.01) mRNA levels and the decreases in Calponin (

0.001) and αSMA (

0.05) mRNA levels in RAVSMCs. Western blotting demonstrated that AMF attenuated the PDGF BB-induced upregulation of MMP2 (

0.001) and MMP9 (

0.001) proteins and the downregulation of Calponin (

0.01) and αSMA (

0.001) proteins. The CCK-8 assay indicated that AMF markedly suppressed PDGFBB-induced excessive proliferation (

0.001)

and wound healing and Transwell assays showed that AMF significantly inhibited PDGFBB-induced cell migration (

0.001). TRRUST transcription factor network analys

is identified RELA (p65) as the top-ranked transcription factor. Western blotting revealed that AMF substantially decreased the phosphorylation level of IκBα (

0.001)

and immunofluorescence staining demonstrated that AMF effectively reduced the nuclear translocation of p65

thereby inhibiting the NF-κB signaling pathway. In the pathway rescue experiment

RT-qPCR showed that TNF-α (20 ng/mL) treatment counteracted the AMF-induced decreases in MMP2 (

=0.087) and MMP9 (

0.05) mRNA levels and the increases in calponin (

0.05) and αSMA (

0.05) mRNA levels. Western blotting confirmed that TNF-α reversed the AMF-mediated reduction in MMP2 (

0.001) and MMP9 (

0.001) protein expression and the elevation of Calponin (

0.05) and αSMA (

=0.063) protein levels.

Conclusion

AMF attenuates AAA progression by targeting the NF-κB-MMP2/9 axis

demonstrating its potential as a novel AAA therapeutic agent.

关键词

Keywords

references

SAKALIHASAN N ， LIMET R ， DEFAWE O . Abdominal aortic aneurysm ［J］. Lancet ， 2005 ， 365 （ 9470 ）： 1577 - 1589 . DOI： 10.1016/S0140-6736（05）66459-8 http://dx.doi.org/10.1016/S0140-6736（05）66459-8 .

BENSON T W ， CONRAD K A ， LI X S ， et al . Gut microbiota-derived trimethylamine N-oxide contributes to abdominal aortic aneurysm through inflammatory and apoptotic mechanisms ［J］. Circulation ， 2023 ， 147 （ 14 ）： 1079 - 1096 . DOI： 10.1161/circulationaha.122.060573 http://dx.doi.org/10.1161/circulationaha.122.060573 .

WEN Y ， LIU Y Y ， LI Q ， et al . Spatiotemporal ATF3 expression determines VSMC fate in abdominal aortic aneurysm ［J］. Circ Res ， 2024 ， 134 （ 11 ）： 1495 - 1511 . DOI： 10.1161/circresaha.124.324323 http://dx.doi.org/10.1161/circresaha.124.324323 .

ZHAO G Z ， ZHAO Y ， LU H C ， et al . BAF60c prevents abdominal aortic aneurysm formation through epigenetic control of vascular smooth muscle cell homeostasis ［J］. J Clin Investig ， 2022 ， 132 （ 21 ）： e158309 . DOI： 10.1172/jci158309 http://dx.doi.org/10.1172/jci158309 .

WANG J ， TIAN X X ， YAN C H ， et al . TCF7L1 accelerates smooth muscle cell phenotypic switching and aggravates abdominal aortic aneurysms ［J］. JACC Basic Transl Sci ， 2023 ， 8 （ 2 ）： 155 - 170 . DOI： 10.1016/j.jacbts.2022.07.012 http://dx.doi.org/10.1016/j.jacbts.2022.07.012 .

ZHANG H D ， YUE H W ， SUN Y J ， et al . Targeting USP21 to inhibit abdominal aortic aneurysm progression by suppressing the phenotypic transition of vascular smooth muscle cells ［J］. Cell Rep Med ， 2025 ， 6 （ 9 ）： 102328 . DOI： 10.1016/j.xcrm.2025.102328 http://dx.doi.org/10.1016/j.xcrm.2025.102328 .

LIU X ， ZHAO L ， LIU D S ， et al . Cytoplasmic and nuclear NFATc3 cooperatively contributes to vascular smooth muscle cell dysfunction and drives aortic aneurysm and dissection ［J］. Acta Pharm Sin B ， 2025 ， 15 （ 7 ）： 3663 - 3684 . DOI： 10.1016/j.apsb.2025.05.016 http://dx.doi.org/10.1016/j.apsb.2025.05.016 .

ZHONG L T ， SUN Y L ， CHEN G J ， et al . Genetic ablation of miR-146a induces abdominal aortic aneurysm formation by intensifying inflammatory M1-like macrophages polarization and vascular smooth muscle cell phenotypic switching ［J］. Arterioscler Thromb Vasc Biol ， 2025 ， 45 （ 12 ）： 2210 - 2225 . DOI： 10.1161/atvbaha.125.322994 http://dx.doi.org/10.1161/atvbaha.125.322994 .

XIONG X F ， TANG N ， LAI X D ， et al . Insights into amentoflavone： a natural multifunctional biflavonoid ［J］. Front Pharmacol ， 2021 ， 12 ： 768708 . DOI： 10.3389/fphar.2021.768708 http://dx.doi.org/10.3389/fphar.2021.768708 .

MENEZES J C J M D S ， DIEDERICH M F . Bioactivity of natural biflavonoids in metabolism-related disease and cancer therapies ［J］. Pharmacol Res ， 2021 ， 167 ： 105525 . DOI： 10.1016/j.phrs.2021.105525 http://dx.doi.org/10.1016/j.phrs.2021.105525 .

FANG G Y ， LI X C ， YANG F Y ， et al . Amentoflavone mitigates doxorubicin-induced cardiotoxicity by suppressing cardiomyocyte pyroptosis and inflammation through inhibition of the STING/NLRP3 signalling pathway ［J］. Phytomedicine ， 2023 ， 117 ： 154922 . DOI： 10.1016/j.phymed.2023.154922 http://dx.doi.org/10.1016/j.phymed.2023.154922 .

ZONG Y ， ZHANG H L . Amentoflavone prevents sepsis-associated acute lung injury through Nrf2-GCLc-mediated upregulation of glutathione ［J］. Acta Biochim Pol ， 2017 ， 64 （ 1 ）： 93 - 98 . DOI： 10.18388/abp.2016_1296 http://dx.doi.org/10.18388/abp.2016_1296 .

DAUGHERTY A ， CASSIS L A . Mouse models of abdominal aortic aneurysms ［J］. Arterioscler Thromb Vasc Biol ， 2004 ， 24 （ 3 ）： 429 - 434 . DOI： 10.1161/01.ATV.0000118013.72016.ea http://dx.doi.org/10.1161/01.ATV.0000118013.72016.ea .

BHAMIDIPATI C M ， MEHTA G S ， LU G Y ， et al . Development of a novel murine model of aortic aneurysms using peri-adventitial elastase ［J］. Surgery ， 2012 ， 152 （ 2 ）： 238 - 246 . DOI： 10.1016/j.surg.2012.02.010 http://dx.doi.org/10.1016/j.surg.2012.02.010 .

YU J Y ， WANG W ， YANG J N ， et al . LncRNA PSR regulates vascular remodeling through encoding a novel protein arteridin ［J］. Circ Res ， 2022 ， 131 （ 9 ）： 768 - 787 . DOI： 10.1161/circresaha.122.321080 http://dx.doi.org/10.1161/circresaha.122.321080 .

SANG W Y ， WANG L ， YAN X J ， et al . Establishment of risk model and analysis of immunoinfiltration based on mitophagy-related associated genes in atrial fibrillation ［J］. J Inflamm Res ， 2023 ， 16 ： 2561 - 2583 . DOI： 10.2147/jir.s415410 http://dx.doi.org/10.2147/jir.s415410 .

MAGUIRE E M ， PEARCE S W A ， XIAO R ， et al . Matrix metalloproteinase in abdominal aortic aneurysm and aortic dissection ［J］. Pharmaceuticals ， 2019 ， 12 （ 3 ）： 118 . DOI： 10.3390/ph12030118 http://dx.doi.org/10.3390/ph12030118 .

FANG L X ， OHASHI K ， OTAKA N ， et al . Omentin attenuates angiotensin II-induced abdominal aortic aneurysm formation in apolipoprotein E-knockout mice ［J］. Cardiovasc Res ， 2022 ， 118 （ 6 ）： 1597 - 1610 . DOI： 10.1093/cvr/cvab179 http://dx.doi.org/10.1093/cvr/cvab179 .

NOSOUDI N ， NAHAR-GOHAD P ， SINHA A ， et al . Prevention of abdominal aortic aneurysm progression by targeted inhibition of matrix metalloproteinase activity with batimastat-loaded nanoparticles ［J］. Circ Res ， 2015 ， 117 （ 11 ）： e80 - e89 . DOI： 10.1161/circresaha.115.307207 http://dx.doi.org/10.1161/circresaha.115.307207 .

SONG T Y ， ZHAO S ， LUO S S ， et al . SLC44A2 regulates vascular smooth muscle cell phenotypic switching and aortic aneurysm ［J］. J Clin Investig ， 2024 ， 134 （ 16 ）： e173690 . DOI： 10.1172/jci173690 http://dx.doi.org/10.1172/jci173690 .

XU Y ， ZHANG H F ， CHEN Y X ， et al . SRF SUMOylation modulates smooth muscle phenotypic switch and vascular remodeling ［J］. Nat Commun ， 2024 ， 15 ： 6919 . DOI： 10.1038/s41467-024-51350-5 http://dx.doi.org/10.1038/s41467-024-51350-5 .

MAO H M ， ZHAO X C ， SUN S C . NF-κB in inflammation and cancer ［J］. Cell Mol Immunol ， 2025 ， 22 （ 8 ）： 811 - 839 . DOI： 10.1038/s41423-025-01310-w http://dx.doi.org/10.1038/s41423-025-01310-w .

YU H ， LIN L B ， ZHANG Z Q ， et al . Targeting NF-κB pathway for the therapy of diseases： mechanism and clinical study ［J］. Signal Transduct Target Ther ， 2020 ， 5 ： 209 . DOI： 10.1038/s41392-020-00312-6 http://dx.doi.org/10.1038/s41392-020-00312-6 .

YOSHIDA T ， YAMASHITA M ， HORIMAI C ， et al . Smooth muscle-selective inhibition of nuclear factor-κB attenuates smooth muscle phenotypic switching and neointima formation following vascular injury ［J］. J Am Heart Assoc ， 2013 ， 2 （ 3 ）： e000230 . DOI： 10.1161/jaha.113.000230 http://dx.doi.org/10.1161/jaha.113.000230 .

ZHANG L ， LENG X X ， QI J X ， et al . The adhesin RadD enhances Fusobacterium nucleatum tumour colonization and colorectal carcinogenesis ［J］. Nat Microbiol ， 2024 ， 9 （ 9 ）： 2292 - 2307 . DOI： 10.1038/s41564-024-01784-w http://dx.doi.org/10.1038/s41564-024-01784-w .

HUANG Y L ， LI G ， LI D ， et al . Ethyl caffeate alleviates inflammatory response and promotes recovery in septic-acute lung injury via the TNF-α/NF-κB/MMP9 axis ［J］. Phytomedicine ， 2025 ， 141 ： 156700 . DOI： 10.1016/j.phymed.2025.156700 http://dx.doi.org/10.1016/j.phymed.2025.156700 .

SONG J H ， HWANG B ， LYEA PARK S ， et al . IL-28A/IL-10Rβ axis promotes angiogenesis via ENOS /AKT signaling and AP-1/NF-κB/MMP-2 network by regulating HSP70-1 expression ［J］. J Adv Res ， 2025 ， 73 ： 247 - 263 . DOI： 10.1016/j.jare.2024.08.013 http://dx.doi.org/10.1016/j.jare.2024.08.013 .

ZHANG J F ， WANG P ， YAN Y J ， et al . IL-33 enhances glioma cell migration and invasion by upregulation of MMP2 and MMP9 via the ST2-NF-κB pathway ［J］. Oncol Rep ， 2017 ， 38 （ 4 ）： 2033 - 2042 . DOI： 10.3892/or.2017.5926 http://dx.doi.org/10.3892/or.2017.5926 .

CHEN F Y ， LI C ， CAO H Y ， et al . Identification of adenylate kinase 5 as a protein target of ginsenosides in brain tissues using mass spectrometry-based drug affinity responsive target stability （DARTS） and cellular thermal shift assay （CETSA） techniques ［J］. J Agric Food Chem ， 2022 ， 70 （ 8 ）： 2741 - 2751 . DOI： 10.1021/acs.jafc.1c07819 http://dx.doi.org/10.1021/acs.jafc.1c07819 .

RAFFORT J ， LAREYRE F ， CLÉMENT M ， et al . Monocytes and macrophages in abdominal aortic aneurysm ［J］. Nat Rev Cardiol ， 2017 ， 14 （ 8 ）： 457 - 471 . DOI： 10.1038/nrcardio.2017.52 http://dx.doi.org/10.1038/nrcardio.2017.52 .

WU X X ， LIU X Y ， CHENG Y Z ， et al . Single-cell RNA sequencing reveals endothelial cell heterogeneity and Sox18-mediated EndMT in abdominal aortic aneurysm ［J］. Theranostics ， 2025 ， 15 （ 18 ）： 9486 - 9507 . DOI： 10.7150/thno.110254 http://dx.doi.org/10.7150/thno.110254 .

ZHAO G Z ， LU H C ， CHANG Z Y ， et al . Single-cell RNA sequencing reveals the cellular heterogeneity of aneurysmal infrarenal abdominal aorta ［J］. Cardiovasc Res ， 2021 ， 117 （ 5 ）： 1402 - 1416 . DOI： 10.1093/cvr/cvaa214 http://dx.doi.org/10.1093/cvr/cvaa214 .

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Related Author

XIA Han

ZHANG Ke

WU Mingdong

HUANG Kai

JIN Qian

LIU Chao

WANG Hongjun

WANG Yong

Related Institution

Department of Cardiovascular Surgery， Second Affiliated Hospital， Army Medical University （Third Military Medical University）

Department of Vascular Surgery， the Second Affiliated Hospital of Chongqing Medical University

School of Basic Medical Sciences， Shanxi Medical University

Chongqing Key Laboratory of Lipid and Glucose Metabolism Disease, Center of Lipid Research, Chongqing Medical University

Department of Anesthesiology, the First Hospital of Lanzhou University

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Amentoflavone attenuates abdominal aortic aneurysm progression by suppressing vascular smooth muscle cell phenotypic switching via targeting NF-κB-MMP2/9 axis

DOI：10.16016/j.2097-0927.202604083

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