• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

尿石素B通过抑制PI3K-AKT信号通路抑制血小板衍生生长因子-BB诱导的血管平滑肌细胞表型转换。

Urolithin B suppresses phenotypic switch in vascular smooth muscle cells induced by PDGF-BB via inhibiting the PI3K-AKT pathway.

作者信息

Li Shengbiao, Zhang Yi, Zhang Tianyi, Jiang Donghui, Li Mi, Chen Ligang, Jiang Jun, Zhang Chunxiang, Li Qiuhong

机构信息

School of Basic Medical Sciences, Southwest Medical University, No. 1 Section 1, Xianglin Road, Longmatan District, Luzhou, 646000, Sichuan, China.

Department of Cardiology, The Affiliated Hospital of Southwest Medical University, Key Laboratory of Medical Electrophysiology, Ministry of Education, Institute of Cardiovascular Research, Basic Medicine Research Innovation Center for Cardiometabolic Diseases, Ministry of Education, Nucleic Acid Medicine of Luzhou Key Laboratory, Southwest Medical University, Luzhou, 646000, Sichuan, China.

出版信息

In Vitro Cell Dev Biol Anim. 2025 Mar;61(3):311-319. doi: 10.1007/s11626-024-01005-y. Epub 2025 Jan 13.

DOI:10.1007/s11626-024-01005-y
PMID:39806237
Abstract

Atherosclerosis (AS) is a prevalent cardiovascular condition, and the growth and phenotypic switch of vascular smooth muscle cells (VSMCs) play a crucial role in its development. Studies have revealed that the activation of certain transcription factors and signaling pathways can trigger these cellular changes. Consequently, targeting these pathways and pivotal molecules has emerged as a promising strategy for AS treatment. Drugs that can reverse the cellular changes in VSMCs may offer new therapeutic options for AS, marking a significant advancement. While previous research has suggested that urolithin B (Uro B) possesses anti-atherosclerotic properties, its exact mechanism remains to be fully understood, especially the effect of Uro B in VSMCs. This study discovered that Uro B can impede the proliferation and migration of VSMCs prompted by PDGF-BB, as well as their phenotypic changes, indicating that Uro B could potentially prevent AS by inhibiting the phenotypic switch of VSMCs.

摘要

动脉粥样硬化(AS)是一种常见的心血管疾病,血管平滑肌细胞(VSMC)的生长和表型转换在其发展过程中起着关键作用。研究表明,某些转录因子和信号通路的激活可引发这些细胞变化。因此,针对这些通路和关键分子已成为一种有前景的AS治疗策略。能够逆转VSMC细胞变化的药物可能为AS提供新的治疗选择,这标志着一项重大进展。虽然先前的研究表明尿石素B(Uro B)具有抗动脉粥样硬化特性,但其确切机制仍有待充分了解,尤其是Uro B对VSMC的影响。本研究发现,Uro B可抑制PDGF-BB诱导的VSMC增殖、迁移及其表型变化,表明Uro B可能通过抑制VSMC的表型转换来预防AS。

相似文献

1
Urolithin B suppresses phenotypic switch in vascular smooth muscle cells induced by PDGF-BB via inhibiting the PI3K-AKT pathway.尿石素B通过抑制PI3K-AKT信号通路抑制血小板衍生生长因子-BB诱导的血管平滑肌细胞表型转换。
In Vitro Cell Dev Biol Anim. 2025 Mar;61(3):311-319. doi: 10.1007/s11626-024-01005-y. Epub 2025 Jan 13.
2
Atorvastatin calcium inhibits phenotypic modulation of PDGF-BB-induced VSMCs via down-regulation the Akt signaling pathway.阿托伐他汀钙通过下调Akt信号通路抑制血小板衍生生长因子BB(PDGF-BB)诱导的血管平滑肌细胞(VSMCs)表型调节。
PLoS One. 2015 Apr 15;10(4):e0122577. doi: 10.1371/journal.pone.0122577. eCollection 2015.
3
Antiproliferative activity of NQ304, a synthetic 1,4-naphthoquinone, is mediated via the suppressions of the PI3K/Akt and ERK1/2 signaling pathways in PDGF-BB-stimulated vascular smooth muscle cells.合成的1,4-萘醌NQ304的抗增殖活性是通过抑制血小板衍生生长因子-BB(PDGF-BB)刺激的血管平滑肌细胞中的PI3K/Akt和ERK1/2信号通路介导的。
Vascul Pharmacol. 2007 Jan;46(1):43-51. doi: 10.1016/j.vph.2006.06.007. Epub 2006 Jun 16.
4
TRIM65 promotes vascular smooth muscle cell phenotypic transformation by activating PI3K/Akt/mTOR signaling during atherogenesis.TRIM65在动脉粥样硬化形成过程中通过激活PI3K/Akt/mTOR信号通路促进血管平滑肌细胞表型转化。
Atherosclerosis. 2024 Mar;390:117430. doi: 10.1016/j.atherosclerosis.2023.117430. Epub 2023 Dec 30.
5
Chicoric acid prevents PDGF-BB-induced VSMC dedifferentiation, proliferation and migration by suppressing ROS/NFκB/mTOR/P70S6K signaling cascade.菊苣酸通过抑制 ROS/NFκB/mTOR/P70S6K 信号级联反应来防止 PDGF-BB 诱导的 VSMC 去分化、增殖和迁移。
Redox Biol. 2018 Apr;14:656-668. doi: 10.1016/j.redox.2017.11.012. Epub 2017 Nov 16.
6
miR-34c inhibits PDGF-BB-induced HAVSMCs phenotypic transformation and proliferation via PDGFR-β/SIRT1 pathway.miR-34c 通过 PDGFR-β/SIRT1 通路抑制 PDGF-BB 诱导的 HAVSMCs 表型转化和增殖。
Mol Biol Rep. 2021 May;48(5):4137-4151. doi: 10.1007/s11033-021-06427-5. Epub 2021 Jun 10.
7
Galangin inhibits neointima formation induced by vascular injury regulating the PI3K/AKT/mTOR pathway.高良姜素通过调控 PI3K/AKT/mTOR 通路抑制血管损伤诱导的新生内膜形成。
Food Funct. 2022 Nov 28;13(23):12077-12092. doi: 10.1039/d2fo02441a.
8
Tangeretin, a citrus flavonoid, inhibits PGDF-BB-induced proliferation and migration of aortic smooth muscle cells by blocking AKT activation.蜜橘素,一种柑橘类黄酮,通过阻断 AKT 激活抑制 PDGF-BB 诱导的主动脉平滑肌细胞增殖和迁移。
Eur J Pharmacol. 2011 Dec 30;673(1-3):56-64. doi: 10.1016/j.ejphar.2011.10.011. Epub 2011 Oct 21.
9
Ketamine, a Clinically Used Anesthetic, Inhibits Vascular Smooth Muscle Cell Proliferation via PP2A-Activated PI3K/Akt/ERK Inhibition.氯胺酮,一种临床应用的麻醉剂,通过激活 PP2A 的 PI3K/Akt/ERK 抑制来抑制血管平滑肌细胞增殖。
Int J Mol Sci. 2017 Nov 27;18(12):2545. doi: 10.3390/ijms18122545.
10
3,3'Diindolylmethane suppresses vascular smooth muscle cell phenotypic modulation and inhibits neointima formation after carotid injury.3,3'-二吲哚甲烷抑制血管平滑肌细胞表型调节并抑制颈动脉损伤后的内膜新生。
PLoS One. 2012;7(4):e34957. doi: 10.1371/journal.pone.0034957. Epub 2012 Apr 10.

本文引用的文献

1
Transcription factors: key regulatory targets of vascular smooth muscle cell in atherosclerosis.转录因子:动脉粥样硬化中血管平滑肌细胞的关键调节靶点。
Mol Med. 2023 Jan 5;29(1):2. doi: 10.1186/s10020-022-00586-2.
2
Recent Advances and Perspectives on the Health Benefits of Urolithin B, A Bioactive Natural Product Derived From Ellagitannins.尿石素B的健康益处的最新进展与展望,尿石素B是一种源自鞣花单宁的生物活性天然产物
Front Pharmacol. 2022 Jun 22;13:917266. doi: 10.3389/fphar.2022.917266. eCollection 2022.
3
Pressure and stiffness sensing together regulate vascular smooth muscle cell phenotype switching.
压力和硬度感知共同调节血管平滑肌细胞表型转换。
Sci Adv. 2022 Apr 15;8(15):eabm3471. doi: 10.1126/sciadv.abm3471.
4
An update on the phenotypic switching of vascular smooth muscle cells in the pathogenesis of atherosclerosis.动脉粥样硬化发病过程中血管平滑肌细胞表型转换的研究进展。
Cell Mol Life Sci. 2021 Dec 22;79(1):6. doi: 10.1007/s00018-021-04079-z.
5
Fate and State of Vascular Smooth Muscle Cells in Atherosclerosis.动脉粥样硬化中血管平滑肌细胞的命运和状态。
Circulation. 2021 May 25;143(21):2110-2116. doi: 10.1161/CIRCULATIONAHA.120.049922. Epub 2021 May 24.
6
Effects of urolithins on obesity-associated gut dysbiosis in rats fed on a high-fat diet.尿石素对高脂肪饮食喂养大鼠肥胖相关肠道菌群失调的影响。
Int J Food Sci Nutr. 2021 Nov;72(7):923-934. doi: 10.1080/09637486.2021.1886255. Epub 2021 Feb 22.
7
Urolithins Attenuate Multiple Symptoms of Obesity in Rats Fed on a High-Fat Diet.尿石素可减轻高脂饮食喂养大鼠的多种肥胖症状。
Diabetes Metab Syndr Obes. 2020 Sep 25;13:3337-3348. doi: 10.2147/DMSO.S268146. eCollection 2020.
8
Urolithin B, a gut microbiota metabolite, protects against myocardial ischemia/reperfusion injury via p62/Keap1/Nrf2 signaling pathway.尿石素 B,一种肠道微生物代谢物,通过 p62/Keap1/Nrf2 信号通路保护心肌免受缺血/再灌注损伤。
Pharmacol Res. 2020 Mar;153:104655. doi: 10.1016/j.phrs.2020.104655. Epub 2020 Jan 26.
9
Urolithin B improves cardiac function and reduces susceptibility to ventricular arrhythmias in rats after myocardial infarction.乌洛托品 B 可改善心肌梗死后大鼠的心脏功能并降低室性心律失常的易感性。
Eur J Pharmacol. 2020 Mar 15;871:172936. doi: 10.1016/j.ejphar.2020.172936. Epub 2020 Jan 17.
10
From Focal Lipid Storage to Systemic Inflammation: JACC Review Topic of the Week.从局灶性脂肪储存到全身炎症:JACC 每周综述专题。
J Am Coll Cardiol. 2019 Sep 24;74(12):1594-1607. doi: 10.1016/j.jacc.2019.07.061.