• 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

血管内皮生长因子B在非酒精性脂肪性肝病中的作用及其潜在价值。

Role of vascular endothelial growth factor B in nonalcoholic fatty liver disease and its potential value.

作者信息

Li Yu-Qi, Xin Lei, Zhao Yu-Chi, Li Shang-Qi, Li Ya-Nuo

机构信息

Department of Pathophysiology, School of Basic Medicine, Binzhou Medical University, Yantai 264000, Shandong Province, China.

Department of Gastrointestinal Surgery, Yantaishan Hospital, Yantai 264000, Shandong Province, China.

出版信息

World J Hepatol. 2023 Jun 27;15(6):786-796. doi: 10.4254/wjh.v15.i6.786.

DOI:10.4254/wjh.v15.i6.786
PMID:37397934
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10308292/
Abstract

Nonalcoholic fatty liver disease (NAFLD) refers to fatty liver disease caused by liver injury factors other than alcohol. The disease is characterized by diffuse fat infiltration, including simple steatosis (no inflammatory fat deposition), nonalcoholic fatty hepatitis, liver fibrosis, and so on, which may cause liver cirrhosis, liver failure, and even liver cancer in the later stage of disease progression. At present, the pathogenesis of NAFLD is still being studied. The "two-hit" theory, represented by lipid metabolism disorder and inflammatory reactions, is gradually enriched by the "multiple-hit" theory, which includes multiple factors, such as insulin resistance and adipocyte dysfunction. In recent years, vascular endothelial growth factor B (VEGFB) has been reported to have the potential to regulate lipid metabolism and is expected to become a novel target for ameliorating metabolic diseases, such as obesity and type 2 diabetes. This review summarizes the regulatory role of VEGFB in the onset and development of NAFLD and illustrates its underlying molecular mechanism. In conclusion, the signaling pathway mediated by VEGFB in the liver may provide an innovative approach to the diagnosis and treatment of NAFLD.

摘要

非酒精性脂肪性肝病(NAFLD)是指由酒精以外的肝脏损伤因素引起的脂肪性肝病。该疾病的特征是弥漫性脂肪浸润,包括单纯性脂肪变性(无炎症性脂肪沉积)、非酒精性脂肪性肝炎、肝纤维化等,在疾病进展后期可能导致肝硬化、肝衰竭,甚至肝癌。目前,NAFLD的发病机制仍在研究中。以脂质代谢紊乱和炎症反应为代表的“二次打击”理论正逐渐被包括胰岛素抵抗和脂肪细胞功能障碍等多种因素的“多次打击”理论所丰富。近年来,有报道称血管内皮生长因子B(VEGFB)具有调节脂质代谢的潜力,有望成为改善肥胖和2型糖尿病等代谢性疾病的新靶点。本文综述了VEGFB在NAFLD发生发展中的调节作用,并阐述了其潜在的分子机制。总之,VEGFB在肝脏中介导的信号通路可能为NAFLD的诊断和治疗提供一种创新方法。

相似文献

1
Role of vascular endothelial growth factor B in nonalcoholic fatty liver disease and its potential value.血管内皮生长因子B在非酒精性脂肪性肝病中的作用及其潜在价值。
World J Hepatol. 2023 Jun 27;15(6):786-796. doi: 10.4254/wjh.v15.i6.786.
2
Reducing VEGFB accelerates NAFLD and insulin resistance in mice via inhibiting AMPK signaling pathway.降低 VEGFB 可通过抑制 AMPK 信号通路加速小鼠的非酒精性脂肪性肝病和胰岛素抵抗。
J Transl Med. 2022 Jul 30;20(1):341. doi: 10.1186/s12967-022-03540-2.
3
The Role of Lipid and Lipoprotein Metabolism in Non-Alcoholic Fatty Liver Disease.脂质和脂蛋白代谢在非酒精性脂肪性肝病中的作用
Children (Basel). 2017 Jun 6;4(6):46. doi: 10.3390/children4060046.
4
Reducing VEGFB expression regulates the balance of glucose and lipid metabolism in mice via VEGFR1.降低 VEGFB 表达通过 VEGFR1 调节小鼠的糖脂代谢平衡。
Mol Med Rep. 2022 Sep;26(3). doi: 10.3892/mmr.2022.12801. Epub 2022 Jul 27.
5
Downregulated microRNA-130b-5p prevents lipid accumulation and insulin resistance in a murine model of nonalcoholic fatty liver disease.下调 microRNA-130b-5p 可预防非酒精性脂肪性肝病小鼠模型中的脂质积累和胰岛素抵抗。
Am J Physiol Endocrinol Metab. 2020 Jul 1;319(1):E34-E42. doi: 10.1152/ajpendo.00528.2019. Epub 2020 Mar 31.
6
Nonalcoholic fatty liver disease and vascular disease: state-of-the-art.非酒精性脂肪性肝病与血管疾病:最新进展
World J Gastroenterol. 2014 Oct 7;20(37):13306-24. doi: 10.3748/wjg.v20.i37.13306.
7
Nonalcoholic fatty liver disease: pathogenesis and the role of antioxidants.非酒精性脂肪性肝病:发病机制及抗氧化剂的作用
Nutr Rev. 2002 Sep;60(9):289-93. doi: 10.1301/002966402320387224.
8
Efficacy of Sitagliptin on Nonalcoholic Fatty Liver Disease in High-fat-diet-fed Diabetic Mice.西他列汀对高脂饮食喂养糖尿病小鼠非酒精性脂肪性肝病的疗效。
Curr Med Sci. 2022 Jun;42(3):513-519. doi: 10.1007/s11596-022-2573-9. Epub 2022 Apr 22.
9
Phytotherapy as Multi-Hit Therapy to Confront the Multiple Pathophysiology in Non-Alcoholic Fatty Liver Disease: A Systematic Review of Experimental Interventions.植物疗法作为一种多靶点治疗方法应对非酒精性脂肪性肝病的多种病理生理学:实验干预的系统评价。
Medicina (Kaunas). 2021 Aug 14;57(8):822. doi: 10.3390/medicina57080822.
10
Nonalcoholic Fatty Liver Disease: An Emerging Modern-Day Risk Factor for Cardiovascular Disease.非酒精性脂肪性肝病:一种新出现的现代心血管疾病风险因素。
Cureus. 2022 May 30;14(5):e25495. doi: 10.7759/cureus.25495. eCollection 2022 May.

引用本文的文献

1
Vascular endothelial growth factor signaling in health and disease: from molecular mechanisms to therapeutic perspectives.健康与疾病中的血管内皮生长因子信号传导:从分子机制到治疗前景
Signal Transduct Target Ther. 2025 May 19;10(1):170. doi: 10.1038/s41392-025-02249-0.
2
VEGFB ameliorates insulin resistance in NAFLD via the PI3K/AKT signal pathway.VEGFB 通过 PI3K/AKT 信号通路改善非酒精性脂肪性肝病的胰岛素抵抗。
J Transl Med. 2024 Oct 28;22(1):976. doi: 10.1186/s12967-024-05621-w.
3
Causal relationship between green tea intake and gastrointestinal disorders: a two-sample Mendelian randomization study.

本文引用的文献

1
Inhibition of VEGF-B signaling prevents non-alcoholic fatty liver disease development by targeting lipolysis in the white adipose tissue.抑制血管内皮生长因子-B信号通路可通过靶向白色脂肪组织中的脂肪分解来预防非酒精性脂肪性肝病的发展。
J Hepatol. 2023 May;78(5):901-913. doi: 10.1016/j.jhep.2023.01.014. Epub 2023 Jan 27.
2
Simultaneous blockade of VEGF-B and IL-17A ameliorated diabetic kidney disease by reducing ectopic lipid deposition and alleviating inflammation response.同时阻断血管内皮生长因子-B(VEGF-B)和白细胞介素-17A(IL-17A)可通过减少异位脂质沉积和减轻炎症反应来改善糖尿病肾病。
Cell Death Discov. 2023 Jan 16;9(1):8. doi: 10.1038/s41420-023-01304-5.
3
绿茶摄入量与胃肠道疾病之间的因果关系:一项两样本孟德尔随机化研究。
Front Nutr. 2024 Sep 20;11:1426779. doi: 10.3389/fnut.2024.1426779. eCollection 2024.
4
Exploring Fibrosis Pathophysiology in Lean and Obese Metabolic-Associated Fatty Liver Disease: An In-Depth Comparison.探讨瘦型和肥胖型代谢相关脂肪性肝病中纤维化发病机制的异同。
Int J Mol Sci. 2024 Jul 5;25(13):7405. doi: 10.3390/ijms25137405.
Reducing VEGFB accelerates NAFLD and insulin resistance in mice via inhibiting AMPK signaling pathway.
降低 VEGFB 可通过抑制 AMPK 信号通路加速小鼠的非酒精性脂肪性肝病和胰岛素抵抗。
J Transl Med. 2022 Jul 30;20(1):341. doi: 10.1186/s12967-022-03540-2.
4
Cardiac-specific VEGFB overexpression reduces lipoprotein lipase activity and improves insulin action in rat heart.心脏特异性 VEGFB 过表达可降低脂蛋白脂肪酶活性并改善大鼠心脏胰岛素作用。
Am J Physiol Endocrinol Metab. 2021 Dec 1;321(6):E753-E765. doi: 10.1152/ajpendo.00219.2021. Epub 2021 Nov 8.
5
Vascular endothelial growth factor B inhibits insulin secretion in MIN6 cells and reduces Ca and cyclic adenosine monophosphate levels through PI3K/AKT pathway.血管内皮生长因子B抑制MIN6细胞中的胰岛素分泌,并通过PI3K/AKT途径降低钙离子和环磷酸腺苷水平。
World J Diabetes. 2021 Apr 15;12(4):480-498. doi: 10.4239/wjd.v12.i4.480.
6
Vascular endothelial growth factor B exerts lipid-lowering effect by activating AMPK via VEGFR1.血管内皮生长因子 B 通过激活 VEGFR1 发挥降脂作用。
Life Sci. 2021 Jul 1;276:119401. doi: 10.1016/j.lfs.2021.119401. Epub 2021 Mar 27.
7
VEGFR1 signaling in retinal angiogenesis and microinflammation.VEGFR1 信号在视网膜血管生成和微炎症中的作用。
Prog Retin Eye Res. 2021 Sep;84:100954. doi: 10.1016/j.preteyeres.2021.100954. Epub 2021 Feb 25.
8
VEGF-B antibody and interleukin-22 fusion protein ameliorates diabetic nephropathy through inhibiting lipid accumulation and inflammatory responses.血管内皮生长因子B抗体与白细胞介素-22融合蛋白通过抑制脂质蓄积和炎症反应改善糖尿病肾病。
Acta Pharm Sin B. 2021 Jan;11(1):127-142. doi: 10.1016/j.apsb.2020.07.002. Epub 2020 Jul 13.
9
Oxidative Stress in Alzheimer's Disease: Therapeutic Effect of Amniotic Fluid Stem Cells Extracellular Vesicles.阿尔茨海默病中的氧化应激:羊水干细胞外泌体的治疗作用
Oxid Med Cell Longev. 2020 Oct 24;2020:2785343. doi: 10.1155/2020/2785343. eCollection 2020.
10
Role of Endoplasmic Reticulum Stress in Atherosclerosis and Its Potential as a Therapeutic Target.内质网应激在动脉粥样硬化中的作用及其作为治疗靶点的潜力。
Oxid Med Cell Longev. 2020 Sep 9;2020:9270107. doi: 10.1155/2020/9270107. eCollection 2020.