• 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

肾小球的机械性挑战与足细胞丢失:一种范式的演变

Mechanical challenges to the glomerulus and podocyte loss: evolution of a paradigm.

作者信息

Lemley Kevin V

机构信息

Department of Pediatrics, University of Southern California Keck School of Medicine, Los Angeles, CA, USA.

Division of Nephrology, Children's Hospital Los Angeles, 4650 Sunset Blvd, MS#40, Los Angeles, CA, 90027, USA.

出版信息

Pflugers Arch. 2017 Aug;469(7-8):959-963. doi: 10.1007/s00424-017-2012-0. Epub 2017 Jun 22.

DOI:10.1007/s00424-017-2012-0
PMID:28643148
Abstract

In this article, I shall outline some of the most important aspects of the evidentiary basis of the so-called Kriz model for the development of glomerular sclerosis, a model that we continue to modify to this day. In my mind, the most important findings include the fact that podocytes are generally post-mitotic cells, so that loss of a significant number for any cause leads to podocyte insufficiency. Another pivotal finding is that in many experimental models and in human disease, podocytes detach from the GBM as living cells. These facts, together with biomechanical deduction, have led to the ongoing evolution of the original Heidelberg model.

摘要

在本文中,我将概述所谓的肾小球硬化症发展的Kriz模型证据基础的一些最重要方面,该模型至今仍在不断修改。在我看来,最重要的发现包括足细胞通常是有丝分裂后细胞,因此任何原因导致大量足细胞丢失都会导致足细胞功能不全。另一个关键发现是,在许多实验模型和人类疾病中,足细胞作为活细胞从肾小球基底膜脱离。这些事实,再加上生物力学推导,导致了原始海德堡模型的不断演变。

相似文献

1
Mechanical challenges to the glomerulus and podocyte loss: evolution of a paradigm.肾小球的机械性挑战与足细胞丢失:一种范式的演变
Pflugers Arch. 2017 Aug;469(7-8):959-963. doi: 10.1007/s00424-017-2012-0. Epub 2017 Jun 22.
2
Similar Biophysical Abnormalities in Glomeruli and Podocytes from Two Distinct Models.肾小球和足细胞的两种不同模型中的类似生物物理异常。
J Am Soc Nephrol. 2018 May;29(5):1501-1512. doi: 10.1681/ASN.2017050475. Epub 2018 Mar 23.
3
Podocyte loss involves MDM2-driven mitotic catastrophe.足细胞丢失涉及 MDM2 驱动的有丝分裂灾难。
J Pathol. 2013 Jul;230(3):322-35. doi: 10.1002/path.4193.
4
[The role of podocytes in normal glomerular function and in the pathogenesis of glomerulonephritis. Part II. Phenotypic and functional changes of podocytes in glomerulonephritis].[足细胞在正常肾小球功能及肾小球肾炎发病机制中的作用。第二部分。肾小球肾炎中足细胞的表型和功能变化]
Postepy Hig Med Dosw (Online). 2006;60:259-64.
5
[The role of podocytes in normal glomerular function and in the pathogenesis of glomerulonephritis. Part I. Phenotypic and functional characteristics of podocytes during their differentiation and maturity].[足细胞在正常肾小球功能及肾小球肾炎发病机制中的作用。第一部分。足细胞分化和成熟过程中的表型及功能特征]
Postepy Hig Med Dosw (Online). 2006;60:248-58.
6
Stressed podocytes-mechanical forces, sensors, signaling and response.应激的足细胞——机械力、传感器、信号传导与反应
Pflugers Arch. 2017 Aug;469(7-8):937-949. doi: 10.1007/s00424-017-2025-8. Epub 2017 Jul 7.
7
A new mouse model of immune-mediated podocyte injury.一种免疫介导的足细胞损伤的新型小鼠模型。
Kidney Int. 2007 Oct;72(7):841-52. doi: 10.1038/sj.ki.5002450. Epub 2007 Jul 25.
8
Podocyte EphB4 signaling helps recovery from glomerular injury.足细胞 EphB4 信号有助于肾小球损伤的恢复。
Kidney Int. 2012 Jun;81(12):1212-25. doi: 10.1038/ki.2012.17. Epub 2012 Mar 7.
9
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.
10
Intrinsic proinflammatory signaling in podocytes contributes to podocyte damage and prolonged proteinuria.足细胞内固有炎症信号通路导致足细胞损伤和蛋白尿迁延不愈。
Am J Physiol Renal Physiol. 2012 Nov 15;303(10):F1473-85. doi: 10.1152/ajprenal.00031.2012. Epub 2012 Sep 12.

引用本文的文献

1
Radiation nephropathy: Mechanisms of injury and recovery in a murine model.放射性肾病:一种小鼠模型中的损伤与修复机制。
Radiother Oncol. 2023 Oct;187:109813. doi: 10.1016/j.radonc.2023.109813. Epub 2023 Jul 17.
2
Glomerular hyperfiltration.肾小球高滤过。
Nat Rev Nephrol. 2022 Jul;18(7):435-451. doi: 10.1038/s41581-022-00559-y. Epub 2022 Apr 1.
3
Control of Podocyte and Glomerular Capillary Wall Structure and Elasticity by WNK1 Kinase.WNK1激酶对足细胞和肾小球毛细血管壁结构及弹性的调控

本文引用的文献

1
Glomerular pathology and the progression of chronic kidney disease.肾小球病理学与慢性肾脏病的进展
Am J Physiol Renal Physiol. 2016 Jun 1;310(11):F1385-8. doi: 10.1152/ajprenal.00099.2016. Epub 2016 Apr 27.
2
Mechanical challenges to the glomerular filtration barrier: adaptations and pathway to sclerosis.肾小球滤过屏障的机械性挑战:适应与硬化途径
Pediatr Nephrol. 2017 Mar;32(3):405-417. doi: 10.1007/s00467-016-3358-9. Epub 2016 Mar 23.
3
A potential role for mechanical forces in the detachment of podocytes and the progression of CKD.
Front Cell Dev Biol. 2021 Feb 2;8:618898. doi: 10.3389/fcell.2020.618898. eCollection 2020.
4
Single-cell transcriptomics reveals gene expression dynamics of human fetal kidney development.单细胞转录组学揭示了人类胎儿肾脏发育的基因表达动态。
PLoS Biol. 2019 Feb 21;17(2):e3000152. doi: 10.1371/journal.pbio.3000152. eCollection 2019 Feb.
5
Similar Biophysical Abnormalities in Glomeruli and Podocytes from Two Distinct Models.肾小球和足细胞的两种不同模型中的类似生物物理异常。
J Am Soc Nephrol. 2018 May;29(5):1501-1512. doi: 10.1681/ASN.2017050475. Epub 2018 Mar 23.
机械力在足细胞脱离及慢性肾脏病进展中的潜在作用。
J Am Soc Nephrol. 2015 Feb;26(2):258-69. doi: 10.1681/ASN.2014030278. Epub 2014 Jul 24.
4
Tensegrity, cellular biophysics, and the mechanics of living systems.张拉整体结构、细胞生物物理学与生命系统的力学
Rep Prog Phys. 2014 Apr;77(4):046603. doi: 10.1088/0034-4885/77/4/046603.
5
The podocyte's response to stress: the enigma of foot process effacement.足细胞对压力的反应:足突融合之谜。
Am J Physiol Renal Physiol. 2013 Feb 15;304(4):F333-47. doi: 10.1152/ajprenal.00478.2012. Epub 2012 Dec 12.
6
The challenge and response of podocytes to glomerular hypertension.足细胞对肾小球高血压的挑战与应对。
Semin Nephrol. 2012 Jul;32(4):327-41. doi: 10.1016/j.semnephrol.2012.06.004.
7
Crk1/2-dependent signaling is necessary for podocyte foot process spreading in mouse models of glomerular disease.Crk1/2 依赖性信号通路对于肾小球疾病小鼠模型中足细胞足突展开是必需的。
J Clin Invest. 2012 Feb;122(2):674-92. doi: 10.1172/JCI60070. Epub 2012 Jan 17.
8
Cumulative excretion of urinary podocytes reflects disease progression in IgA nephropathy and Schönlein-Henoch purpura nephritis.尿足细胞的累积排泄反映了IgA肾病和过敏性紫癜性肾炎的疾病进展。
Clin J Am Soc Nephrol. 2007 Mar;2(2):231-8. doi: 10.2215/CJN.01470506. Epub 2007 Jan 31.
9
Podocytes are sensitive to fluid shear stress in vitro.足细胞在体外对流体剪切应力敏感。
Am J Physiol Renal Physiol. 2006 Oct;291(4):F856-65. doi: 10.1152/ajprenal.00196.2005. Epub 2006 May 9.
10
Podocyte depletion causes glomerulosclerosis: diphtheria toxin-induced podocyte depletion in rats expressing human diphtheria toxin receptor transgene.足细胞耗竭导致肾小球硬化:白喉毒素诱导表达人白喉毒素受体转基因大鼠的足细胞耗竭。
J Am Soc Nephrol. 2005 Oct;16(10):2941-52. doi: 10.1681/ASN.2005010055. Epub 2005 Aug 17.