• 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

中医药干预PI3K/AKT信号通路调控纤维化的研究进展

Review of Chinese medicine intervention in PI3K/AKT pathway to regulate fibrosis.

作者信息

Huang Shu-Ping, Zhang Ze-Chao, Chen Yu, Shang Chang-Jie, Zhu Min, Li Wei-Hong

机构信息

Department of Traditional Chinese Medicine Surgery, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, China.

Department of Yao College of Medicine and Graduate School, Guangxi University of Chinese Medicine, Nanning, China.

出版信息

Medicine (Baltimore). 2025 Jul 11;104(28):e42957. doi: 10.1097/MD.0000000000042957.

DOI:10.1097/MD.0000000000042957
PMID:40660593
Abstract

The phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway plays a crucial role in the regulation of fibrosis, a pathological process characterized by excessive deposition of extracellular matrix components leading to tissue scarring and dysfunction. Traditional Chinese medicine (TCM) has been increasingly recognized for its potential therapeutic effects in fibrosis by targeting various signaling pathways, including the PI3K/AKT pathway. This review aims to summarize the recent advancements in TCM interventions targeting the PI3K/AKT signaling pathway for the regulation of fibrotic diseases. Recent studies have explored the potential of TCM in the prevention and treatment of fibrotic diseases, particularly through the modulation of the PI3K/AKT signaling pathway. To gather information on TCM and the PI3K/AKT pathway, an extensive search was conducted across various scientific databases, such as Google Scholar, Web of Science, Scifinder, Baidu Scholar and PubMed. TCM has demonstrated unique potential in managing fibrotic diseases through the modulation of the PI3K/AKT signaling pathway. About 37 types of TCM monomers, 68 species of extracts and related compounds, and 50 types of TCM formulas. It discusses their treatment effects on fibrosis in various organs by regulating the PI3K/AKT pathway. The current advancements in TCM interventions targeting the PI3K/AKT pathway offer novel perspectives and strategies for the management of fibrotic diseases. TCM has shown positive effects in treating fibrotic diseases.

摘要

磷脂酰肌醇-3-激酶(PI3K)/蛋白激酶B(AKT)信号通路在纤维化调节中起关键作用,纤维化是一种以细胞外基质成分过度沉积导致组织瘢痕形成和功能障碍为特征的病理过程。中药因其通过靶向包括PI3K/AKT通路在内的各种信号通路在纤维化治疗中的潜在疗效而日益受到认可。本综述旨在总结中药干预PI3K/AKT信号通路调节纤维化疾病的最新进展。最近的研究探索了中药在预防和治疗纤维化疾病方面的潜力,特别是通过调节PI3K/AKT信号通路。为了收集有关中药和PI3K/AKT通路的信息,我们在多个科学数据库中进行了广泛搜索,如谷歌学术、科学网、Scifinder、百度学术和PubMed。中药已证明通过调节PI3K/AKT信号通路在管理纤维化疾病方面具有独特潜力。约37种中药单体、68种提取物及相关化合物以及50种中药方剂。它讨论了它们通过调节PI3K/AKT通路对各器官纤维化的治疗作用。目前针对PI3K/AKT通路的中药干预进展为纤维化疾病的管理提供了新的视角和策略。中药在治疗纤维化疾病方面已显示出积极效果。

相似文献

1
Review of Chinese medicine intervention in PI3K/AKT pathway to regulate fibrosis.中医药干预PI3K/AKT信号通路调控纤维化的研究进展
Medicine (Baltimore). 2025 Jul 11;104(28):e42957. doi: 10.1097/MD.0000000000042957.
2
Targeting ferroptosis using Chinese herbal compounds to treat respiratory diseases.利用中草药化合物靶向铁死亡治疗呼吸疾病。
Phytomedicine. 2024 Jul 25;130:155738. doi: 10.1016/j.phymed.2024.155738. Epub 2024 Jun 1.
3
Research progress of effective components of traditional Chinese medicine in intervening apoptosis of renal tubular epithelial cells in diabetic kidney disease.中药有效成分干预糖尿病肾病肾小管上皮细胞凋亡的研究进展
J Ethnopharmacol. 2025 May 28;348:119874. doi: 10.1016/j.jep.2025.119874. Epub 2025 Apr 23.
4
Bioactive fraction of processed Curcumae Rhizoma-Sparganii Rhizoma anti-liver fibrosis by regulate taurine metabolism through PI3K/AKT pathway.制莪术-三棱的生物活性成分通过PI3K/AKT途径调节牛磺酸代谢来抗肝纤维化。
J Ethnopharmacol. 2025 Jul 24;351:120090. doi: 10.1016/j.jep.2025.120090. Epub 2025 Jun 3.
5
Urolithin A attenuates pulmonary fibrosis via the PI3K/AKT/mTOR pathway: Evidence from network pharmacology and experimental validation.尿石素A通过PI3K/AKT/mTOR途径减轻肺纤维化:来自网络药理学和实验验证的证据。
Biochem Biophys Res Commun. 2025 Jun 17;776:152219. doi: 10.1016/j.bbrc.2025.152219.
6
Targeting ferroptosis in the treatment of ulcerative colitis by traditional Chinese medicine: A novel therapeutic strategies.中药靶向铁死亡治疗溃疡性结肠炎:一种新的治疗策略
Phytomedicine. 2025 Apr;139:156539. doi: 10.1016/j.phymed.2025.156539. Epub 2025 Feb 17.
7
[Alpiniae Oxyphyllae Fructus-Saposhnikoviae Radix regulates NLRP3 inflammasome to ameliorate inflammatory response in diabetic kidney disease mice through PI3K/Akt/mTOR signaling pathway].[益智-防风调控NLRP3炎性小体通过PI3K/Akt/mTOR信号通路改善糖尿病肾病小鼠的炎症反应]
Zhongguo Zhong Yao Za Zhi. 2025 May;50(10):2798-2809. doi: 10.19540/j.cnki.cjcmm.20250214.502.
8
Chinese Medicine for Non-Alcoholic Fatty Liver Disease: Targeting Key Signaling Pathways.用于非酒精性脂肪性肝病的中药:靶向关键信号通路
Am J Chin Med. 2025;53(5):1379-1410. doi: 10.1142/S0192415X25500533. Epub 2025 Jul 18.
9
Gut microbiota: A new target for traditional Chinese medicine in the treatment of depression.肠道微生物群:中医药治疗抑郁症的新靶点。
J Ethnopharmacol. 2023 Mar 1;303:116038. doi: 10.1016/j.jep.2022.116038. Epub 2022 Dec 15.
10
Shikonin Inhibits the Migration and Invasion of Human Glioblastoma Cells by Targeting Phosphorylated β-Catenin and Phosphorylated PI3K/Akt: A Potential Mechanism for the Anti-Glioma Efficacy of a Traditional Chinese Herbal Medicine.紫草素通过靶向磷酸化β-连环蛋白和磷酸化PI3K/Akt抑制人胶质母细胞瘤细胞的迁移和侵袭:一种传统中药抗胶质瘤疗效的潜在机制。
Int J Mol Sci. 2015 Oct 9;16(10):23823-48. doi: 10.3390/ijms161023823.

本文引用的文献

1
Baicalin attenuates pulmonary vascular remodeling by inhibiting calpain-1 mediated endothelial-to-mesenchymal transition.黄芩苷通过抑制钙蛋白酶-1介导的内皮-间充质转化减轻肺血管重塑。
Heliyon. 2023 Nov 30;9(12):e23076. doi: 10.1016/j.heliyon.2023.e23076. eCollection 2023 Dec.
2
[Mechanism of Wuling Capsules against hepatic fibrosis based on network pharmacology and animal experiments].基于网络药理学和动物实验的五灵胶囊抗肝纤维化机制研究
Zhongguo Zhong Yao Za Zhi. 2023 Oct;48(19):5365-5376. doi: 10.19540/j.cnki.cjcmm.20230707.501.
3
Therapeutic potential for renal fibrosis by targeting Smad3-dependent noncoding RNAs.
靶向 Smad3 依赖性非编码 RNA 治疗肾纤维化的潜力。
Mol Ther. 2024 Feb 7;32(2):313-324. doi: 10.1016/j.ymthe.2023.12.009. Epub 2023 Dec 12.
4
Programmed cell death in hepatic fibrosis: current and perspectives.肝纤维化中的程序性细胞死亡:现状与展望
Cell Death Discov. 2023 Dec 12;9(1):449. doi: 10.1038/s41420-023-01749-8.
5
Titanium Dioxide Nanoparticles Induce Cell Cycle Arrest and Apoptosis through Inhibiting PI3K/AKT/mTOR Pathway in Spermatogonia.二氧化钛纳米颗粒通过抑制精原细胞中的 PI3K/AKT/mTOR 通路诱导细胞周期停滞和凋亡。
Biol Trace Elem Res. 2024 Sep;202(9):4065-4077. doi: 10.1007/s12011-023-03984-7. Epub 2023 Dec 11.
6
Modified Guo-Min decoction ameliorates PM2.5-induced lung injury by inhibition of PI3K-AKT and MAPK signaling pathways.改良过的郭氏方剂通过抑制 PI3K-AKT 和 MAPK 信号通路来改善 PM2.5 引起的肺损伤。
Phytomedicine. 2024 Jan;123:155211. doi: 10.1016/j.phymed.2023.155211. Epub 2023 Nov 23.
7
Salidroside attenuates myocardial remodeling in DOCA-salt-induced mice by inhibiting the endothelin 1 and PI3K/AKT/NFκB signaling pathways.红景天苷通过抑制内皮素 1 和 PI3K/AKT/NFκB 信号通路减轻 DOCA-盐诱导的小鼠心肌重构。
Eur J Pharmacol. 2024 Jan 5;962:176236. doi: 10.1016/j.ejphar.2023.176236. Epub 2023 Dec 2.
8
Synergistic effects of T-2 toxin and selenium deficiency exacerbate renal fibrosis through modulation of the ERα/PI3K/Akt signaling pathway.T-2 毒素与硒缺乏的协同作用通过调节 ERα/PI3K/Akt 信号通路加剧肾纤维化。
Ecotoxicol Environ Saf. 2024 Jan 1;269:115748. doi: 10.1016/j.ecoenv.2023.115748. Epub 2023 Nov 28.
9
The mechanism of Shenbing Decoction II against IgA nephropathy renal fibrosis revealed by UPLC-MS/MS, network pharmacology and experimental verification.超高效液相色谱-串联质谱联用、网络药理学及实验验证揭示肾痹汤Ⅱ号抗IgA肾病肾纤维化的机制
Heliyon. 2023 Nov 3;9(11):e21997. doi: 10.1016/j.heliyon.2023.e21997. eCollection 2023 Nov.
10
Hepatoprotective Effect of Medicine Food Homology Flower Saffron against CCl-Induced Liver Fibrosis in Mice via the Akt/HIF-1α/VEGF Signaling Pathway.药食同源西红花通过 Akt/HIF-1α/VEGF 信号通路对 CCl4 诱导的肝纤维化的保护作用。
Molecules. 2023 Oct 24;28(21):7238. doi: 10.3390/molecules28217238.