• 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

迁移小体和外泌体;足细胞中不同类型的信息传递囊泡。

Migrasomes and exosomes; different types of messaging vesicles in podocytes.

机构信息

Kidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

Noncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran.

出版信息

Cell Biol Int. 2022 Jan;46(1):52-62. doi: 10.1002/cbin.11711. Epub 2021 Oct 21.

DOI:10.1002/cbin.11711
PMID:34647672
Abstract

Podocytes, highly specified kidney epithelial cells, live under several pathological stimuli and stresses during which they adapt themselves to keep homeostasis. Nevertheless, under extreme stress, a complex scenario of podocyte damage and its consequences occur. Podocyte damage causes foot process effacement and their detachment from the glomerular basement membrane, leading to proteinuria. Podocyte-derived extracellular vesicles (pEVs), mainly microparticles and exosomes are considered as signaling mediators of intercellular communication. Recently, it has been shown that throughout the injury-related migration procedure, podocytes are capable of releasing the injury-related migrasomes. Evidence indicates that at the early stages of glomerular disorders, increased levels of pEVs are observed in urine. At the early stage of nephropathy, pEVs especially migrasomes seem to be more sensitive and reliable indicators of podocyte stress and/or damage than proteinuria. This review highlights the current knowledge of pEVs and their values for the diagnosis of different kidney diseases.

摘要

足细胞是高度特化的肾脏上皮细胞,在多种病理刺激和应激下生存,在此期间它们会自我适应以保持体内平衡。然而,在极端应激下,会发生复杂的足细胞损伤及其后果。足细胞损伤导致足突融合和它们与肾小球基底膜的分离,导致蛋白尿。足细胞来源的细胞外囊泡(pEVs),主要是微颗粒和外泌体,被认为是细胞间通讯的信号介质。最近,已经表明,在与损伤相关的迁移过程中,足细胞能够释放损伤相关的迁移体。有证据表明,在肾小球疾病的早期阶段,尿液中 pEVs 的水平升高。在肾脏病的早期阶段,pEVs 特别是迁移体似乎比蛋白尿更能敏感和可靠地反映足细胞的应激和/或损伤。本综述强调了 pEVs 的最新知识及其在诊断不同肾脏疾病中的价值。

相似文献

1
Migrasomes and exosomes; different types of messaging vesicles in podocytes.迁移小体和外泌体;足细胞中不同类型的信息传递囊泡。
Cell Biol Int. 2022 Jan;46(1):52-62. doi: 10.1002/cbin.11711. Epub 2021 Oct 21.
2
Podocyte-Released Migrasomes in Urine Serve as an Indicator for Early Podocyte Injury.尿液中足细胞释放的迁移小体可作为早期足细胞损伤的指标。
Kidney Dis (Basel). 2020 Nov;6(6):422-433. doi: 10.1159/000511504. Epub 2020 Oct 23.
3
Contribution of podocyte inflammatory exosome release to glomerular inflammation and sclerosis during hyperhomocysteinemia.高同型半胱氨酸血症时足细胞炎症外泌体释放对肾小球炎症和硬化的贡献。
Biochim Biophys Acta Mol Basis Dis. 2021 Jul 1;1867(7):166146. doi: 10.1016/j.bbadis.2021.166146. Epub 2021 Apr 14.
4
Quantification of urinary podocyte-derived migrasomes for the diagnosis of kidney disease.尿足细胞来源迁移小体定量用于肾脏疾病的诊断。
J Extracell Vesicles. 2024 Jun;13(6):e12460. doi: 10.1002/jev2.12460.
5
Urinary exosomal Wilms' tumor-1 as a potential biomarker for podocyte injury.尿外泌体 Wilms' 肿瘤-1 作为足细胞损伤的潜在生物标志物。
Am J Physiol Renal Physiol. 2013 Aug 15;305(4):F553-9. doi: 10.1152/ajprenal.00056.2013. Epub 2013 Jun 12.
6
Mitochondrial dysfunction is an early event in aldosterone-induced podocyte injury.线粒体功能障碍是醛固酮诱导足细胞损伤的早期事件。
Am J Physiol Renal Physiol. 2013 Aug 15;305(4):F520-31. doi: 10.1152/ajprenal.00570.2012. Epub 2013 Jun 12.
7
Podocyte injury and its consequences.足细胞损伤及其后果。
Kidney Int. 2016 Jun;89(6):1221-30. doi: 10.1016/j.kint.2016.01.012. Epub 2016 Mar 19.
8
Dipping your feet in the water: podocytes in urine.将双脚浸入水中:尿液中的足细胞。
Expert Rev Mol Diagn. 2014 May;14(4):423-37. doi: 10.1586/14737159.2014.908122. Epub 2014 Apr 11.
9
Fn14 in podocytes and proteinuric kidney disease.足细胞中的Fn14与蛋白尿性肾病
Biochim Biophys Acta. 2013 Dec;1832(12):2232-43. doi: 10.1016/j.bbadis.2013.08.010. Epub 2013 Aug 30.
10
Signaling in regulation of podocyte phenotypes.足细胞表型调控中的信号传导。
Nephron Physiol. 2009;111(2):p9-15. doi: 10.1159/000191075. Epub 2009 Jan 13.

引用本文的文献

1
Migrasomes, critical players in intercellular communication.迁移小体,细胞间通讯的关键参与者。
Cancer Cell Int. 2025 Mar 25;25(1):113. doi: 10.1186/s12935-025-03754-6.
2
Migrasomes: Biogenesis, physiological roles, and therapeutic potentials.迁移体:发生、生理作用和治疗潜力。
J Cell Biol. 2024 Nov 4;223(11). doi: 10.1083/jcb.202403051. Epub 2024 Oct 14.
3
Research progress of migrasomes: from genesis to formation, physiology to pathology.迁移小体的研究进展:从起源到形成,从生理到病理
Front Cell Dev Biol. 2024 Aug 14;12:1420413. doi: 10.3389/fcell.2024.1420413. eCollection 2024.
4
Future embracing: exosomes driving a revolutionary approach to the diagnosis and treatment of idiopathic membranous nephropathy.拥抱未来:外泌体推动特发性膜性肾病诊断和治疗的革命性方法。
J Nanobiotechnology. 2024 Aug 8;22(1):472. doi: 10.1186/s12951-024-02633-y.
5
Podocyte-specific proteins in urinary extracellular vesicles of patients with IgA nephropathy: Vasorin and ceruloplasmin.IgA肾病患者尿细胞外囊泡中的足细胞特异性蛋白:血管紧张素原和铜蓝蛋白。
Bioimpacts. 2024;14(3):29981. doi: 10.34172/bi.2023.29981. Epub 2023 Oct 31.
6
CD151-enriched migrasomes mediate hepatocellular carcinoma invasion by conditioning cancer cells and promoting angiogenesis.富含 CD151 的迁移小体通过调节癌细胞和促进血管生成来介导肝细胞癌侵袭。
J Exp Clin Cancer Res. 2024 Jun 6;43(1):160. doi: 10.1186/s13046-024-03082-z.
7
Migrasome: a new functional extracellular vesicle.迁移体:一种新型功能性细胞外囊泡。
Cell Death Discov. 2023 Oct 18;9(1):381. doi: 10.1038/s41420-023-01673-x.
8
Migrasome, a novel organelle, differs from exosomes.迁移小体是一种新型细胞器,与外泌体不同。
Biochem Biophys Rep. 2023 Jun 9;35:101500. doi: 10.1016/j.bbrep.2023.101500. eCollection 2023 Sep.
9
Migrasomes, new vescicles as Hansel and Gretel white pebbles?迁移体,作为汉塞尔与格蕾特的白色鹅卵石的新型小泡?
Biol Direct. 2022 Apr 28;17(1):8. doi: 10.1186/s13062-022-00321-1.
10
Migrasomes: From Biogenesis, Release, Uptake, Rupture to Homeostasis and Diseases.迁移体:从生物发生、释放、摄取、破裂到动态平衡和疾病。
Oxid Med Cell Longev. 2022 Apr 14;2022:4525778. doi: 10.1155/2022/4525778. eCollection 2022.