• 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

糖尿病肾病中的蛋白质甲基化

Protein Methylation in Diabetic Kidney Disease.

作者信息

Cheng Ye, Chen Yanna, Wang Guodong, Liu Pei, Xie Guiling, Jing Huan, Chen Hongtao, Fan Youlin, Wang Min, Zhou Jun

机构信息

Department of Anesthesiology, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.

Department of Anesthesiology, The Eighth People's Hospital of Guangzhou, Guangzhou, China.

出版信息

Front Med (Lausanne). 2022 May 12;9:736006. doi: 10.3389/fmed.2022.736006. eCollection 2022.

DOI:10.3389/fmed.2022.736006
PMID:35647002
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9133329/
Abstract

Chronic kidney disease (CKD) is defined by persistent urine aberrations, structural abnormalities, or impaired excretory renal function. Diabetes is the leading cause of CKD. Their common pathological manifestation is renal fibrosis. Approximately half of all patients with type 2 diabetes and one-third with type 1 diabetes will develop CKD. However, renal fibrosis mechanisms are still poorly understood, especially post-transcriptional and epigenetic regulation. And an unmet need remains for innovative treatment strategies for preventing, arresting, treating, and reversing diabetic kidney disease (DKD). People believe that protein methylation, including histone and non-histone, is an essential type of post-translational modification (PTM). However, prevalent reviews mainly focus on the causes such as DNA methylation. This review will take insights into the protein part. Furthermore, by emphasizing the close relationship between protein methylation and DKD, we will summarize the clinical research status and foresee the application prospect of protein methyltransferase (PMT) inhibitors in DKD treatment. In a nutshell, our review will contribute to a more profound understanding of DKD's molecular mechanism and inspire people to dig into this field.

摘要

慢性肾脏病(CKD)的定义为持续性尿液异常、结构异常或肾脏排泄功能受损。糖尿病是CKD的主要病因。它们共同的病理表现是肾纤维化。大约一半的2型糖尿病患者和三分之一的1型糖尿病患者会发展为CKD。然而,肾纤维化机制仍未被充分了解,尤其是转录后和表观遗传调控方面。对于预防、阻止、治疗和逆转糖尿病肾病(DKD)的创新治疗策略仍存在未满足的需求。人们认为蛋白质甲基化,包括组蛋白和非组蛋白甲基化,是一种重要的翻译后修饰(PTM)类型。然而,目前流行的综述主要关注DNA甲基化等原因。本综述将深入探讨蛋白质部分。此外,通过强调蛋白质甲基化与DKD之间的密切关系,我们将总结临床研究现状并展望蛋白质甲基转移酶(PMT)抑制剂在DKD治疗中的应用前景。简而言之,我们的综述将有助于更深入地理解DKD的分子机制,并激励人们深入研究该领域。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e99/9133329/265cddc507bc/fmed-09-736006-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e99/9133329/36aab4d4d9d2/fmed-09-736006-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e99/9133329/0baa7189a5c2/fmed-09-736006-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e99/9133329/265cddc507bc/fmed-09-736006-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e99/9133329/36aab4d4d9d2/fmed-09-736006-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e99/9133329/0baa7189a5c2/fmed-09-736006-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e99/9133329/265cddc507bc/fmed-09-736006-g003.jpg

相似文献

1
Protein Methylation in Diabetic Kidney Disease.糖尿病肾病中的蛋白质甲基化
Front Med (Lausanne). 2022 May 12;9:736006. doi: 10.3389/fmed.2022.736006. eCollection 2022.
2
Histone methylation modification and diabetic kidney disease: Potential molecular mechanisms and therapeutic approaches (Review).组蛋白甲基化修饰与糖尿病肾病:潜在的分子机制和治疗方法(综述)。
Int J Mol Med. 2024 Nov;54(5). doi: 10.3892/ijmm.2024.5428. Epub 2024 Sep 20.
3
Epigenetic Histone Modifications in the Pathogenesis of Diabetic Kidney Disease.表观遗传组蛋白修饰在糖尿病肾病发病机制中的作用
Diabetes Metab Syndr Obes. 2021 Jan 22;14:329-344. doi: 10.2147/DMSO.S288500. eCollection 2021.
4
Prognostic imaging biomarkers for diabetic kidney disease (iBEAt): study protocol.糖尿病肾病(iBEAt)的预后成像生物标志物:研究方案。
BMC Nephrol. 2020 Jun 29;21(1):242. doi: 10.1186/s12882-020-01901-x.
5
Epigenetics and epigenomics in diabetic kidney disease and metabolic memory.糖尿病肾病和代谢记忆中的表观遗传学和表观基因组学。
Nat Rev Nephrol. 2019 Jun;15(6):327-345. doi: 10.1038/s41581-019-0135-6.
6
Epigenetic Modification Mechanisms Involved in Inflammation and Fibrosis in Renal Pathology.在肾脏病理学中涉及炎症和纤维化的表观遗传修饰机制。
Mediators Inflamm. 2018 Dec 13;2018:2931049. doi: 10.1155/2018/2931049. eCollection 2018.
7
Role of Epigenetic Histone Modifications in Diabetic Kidney Disease Involving Renal Fibrosis.表观遗传组蛋白修饰在涉及肾纤维化的糖尿病肾病中的作用
J Diabetes Res. 2017;2017:7242384. doi: 10.1155/2017/7242384. Epub 2017 Jun 13.
8
TGFβ-incurred epigenetic aberrations of miRNA and DNA methyltransferase suppress Klotho and potentiate renal fibrosis.TGFβ 诱导的 miRNA 和 DNA 甲基转移酶表观遗传异常抑制 Klotho 并促进肾纤维化。
Biochim Biophys Acta Mol Cell Res. 2017 Jul;1864(7):1207-1216. doi: 10.1016/j.bbamcr.2017.03.002. Epub 2017 Mar 7.
9
Mechanisms of metabolic memory and renal hypoxia as a therapeutic target in diabetic kidney disease.代谢记忆机制及肾缺氧作为糖尿病肾病的治疗靶点
J Diabetes Investig. 2017 May;8(3):261-271. doi: 10.1111/jdi.12624. Epub 2017 Mar 13.
10
RNA-binding proteins tristetraprolin and human antigen R are novel modulators of podocyte injury in diabetic kidney disease.RNA 结合蛋白 tristetraprolin 和人抗原 R 是糖尿病肾病中足细胞损伤的新型调节因子。
Cell Death Dis. 2020 Jun 2;11(6):413. doi: 10.1038/s41419-020-2630-x.

引用本文的文献

1
DNMT3B aggravated renal fibrosis in diabetic kidney disease via activating Wnt/β-catenin signaling pathway.DNMT3B通过激活Wnt/β-连环蛋白信号通路加重糖尿病肾病中的肾纤维化。
Sci Rep. 2025 Jul 1;15(1):21070. doi: 10.1038/s41598-025-06713-3.
2
Multiplatform Metabolomic Profiling of the Unilateral Ureteral Obstruction Murine Model of CKD.慢性肾脏病单侧输尿管梗阻小鼠模型的多平台代谢组学分析
Int J Mol Sci. 2025 May 21;26(10):4933. doi: 10.3390/ijms26104933.
3
Neddylation of RhoA impairs its protein degradation and promotes renal interstitial fibrosis progression in diabetic nephropathy.

本文引用的文献

1
ets1 associates with KMT5A to participate in high glucose-mediated EndMT via upregulation of PFN2 expression in diabetic nephropathy.ets1 通过上调 PFN2 表达参与高糖介导的 EndMT,进而与 KMT5A 相互作用在糖尿病肾病中。
Mol Med. 2021 Jul 8;27(1):74. doi: 10.1186/s10020-021-00339-7.
2
Critical roles of SMYD2 lysine methyltransferase in mediating renal fibroblast activation and kidney fibrosis.SMYD2 赖氨酸甲基转移酶在介导肾成纤维细胞活化和肾脏纤维化中的关键作用。
FASEB J. 2021 Jul;35(7):e21715. doi: 10.1096/fj.202000554RRR.
3
Pharmacological inhibition of SETD7 by PFI-2 attenuates renal fibrosis following folic acid and obstruction injury.
RhoA的Neddylation修饰会损害其蛋白质降解,并促进糖尿病肾病中肾间质纤维化的进展。
Acta Pharmacol Sin. 2025 Jun;46(6):1692-1705. doi: 10.1038/s41401-024-01460-z. Epub 2025 Feb 3.
4
Histone methylation modification and diabetic kidney disease: Potential molecular mechanisms and therapeutic approaches (Review).组蛋白甲基化修饰与糖尿病肾病:潜在的分子机制和治疗方法(综述)。
Int J Mol Med. 2024 Nov;54(5). doi: 10.3892/ijmm.2024.5428. Epub 2024 Sep 20.
5
Risk factors for chronic kidney disease progression over 20 years for primary prevention in Japanese individuals at a preventive medicine research center: Focus on the influence of plasma glucose levels.20 年期间日本个体在预防医学研究中心进行原发性预防的慢性肾脏病进展的风险因素:关注血浆葡萄糖水平的影响。
J Diabetes Investig. 2024 Oct;15(10):1434-1443. doi: 10.1111/jdi.14259. Epub 2024 Jul 2.
6
Targeted deletion of von-Hippel-Lindau in the proximal tubule conditions the kidney against early diabetic kidney disease.靶向敲除近端肾小管中的 von-Hippel-Lindau 可预防早期糖尿病肾病。
Cell Death Dis. 2023 Aug 26;14(8):562. doi: 10.1038/s41419-023-06074-7.
7
Protein posttranslational modifications in health and diseases: Functions, regulatory mechanisms, and therapeutic implications.健康与疾病中的蛋白质翻译后修饰:功能、调控机制及治疗意义
MedComm (2020). 2023 May 2;4(3):e261. doi: 10.1002/mco2.261. eCollection 2023 Jun.
8
Stratification of diabetic kidney diseases data-independent acquisition proteomics-based analysis of human kidney tissue specimens.基于数据非依赖采集的人类肾组织标本蛋白质组学分析对糖尿病肾脏疾病进行分层。
Front Endocrinol (Lausanne). 2022 Nov 17;13:995362. doi: 10.3389/fendo.2022.995362. eCollection 2022.
PFI-2对SETD7的药理学抑制作用可减轻叶酸和梗阻性损伤后的肾纤维化。
Eur J Pharmacol. 2021 Jun 15;901:174097. doi: 10.1016/j.ejphar.2021.174097. Epub 2021 Apr 19.
4
The CREB/KMT5A complex regulates PTP1B to modulate high glucose-induced endothelial inflammatory factor levels in diabetic nephropathy.CREB/KMT5A复合物通过调节蛋白酪氨酸磷酸酶1B来调控糖尿病肾病中高糖诱导的内皮炎症因子水平。
Cell Death Dis. 2021 Mar 29;12(4):333. doi: 10.1038/s41419-021-03629-4.
5
Emodin ameliorates tubulointerstitial fibrosis in obstructed kidneys by inhibiting EZH2.大黄素通过抑制 EZH2 改善梗阻性肾病的肾小管间质纤维化。
Biochem Biophys Res Commun. 2021 Jan 1;534:279-285. doi: 10.1016/j.bbrc.2020.11.094. Epub 2020 Dec 4.
6
Role of SET7/9 in the progression of ischemic renal injury in diabetic and non-diabetic rats.SET7/9 在糖尿病和非糖尿病大鼠缺血性肾损伤进展中的作用。
Biochem Biophys Res Commun. 2020 Jul 12;528(1):14-20. doi: 10.1016/j.bbrc.2020.05.075. Epub 2020 May 22.
7
Inhibition of Disruptor of Telomeric Silencing 1-Like Alleviated Renal Ischemia and Reperfusion Injury-Induced Fibrosis by Blocking PI3K/AKT-Mediated Oxidative Stress.抑制端粒沉默破坏因子1样蛋白通过阻断PI3K/AKT介导的氧化应激减轻肾缺血再灌注损伤诱导的纤维化。
Drug Des Devel Ther. 2019 Dec 27;13:4375-4387. doi: 10.2147/DDDT.S224909. eCollection 2019.
8
Regeneration after acute kidney injury requires PTIP-mediated epigenetic modifications.急性肾损伤后的再生需要 PTIP 介导的表观遗传修饰。
JCI Insight. 2020 Feb 13;5(3):130204. doi: 10.1172/jci.insight.130204.
9
Protein arginine methyltransferase 1 mediates renal fibroblast activation and fibrogenesis through activation of Smad3 signaling.精氨酸甲基转移酶 1 通过激活 Smad3 信号转导介导肾小管间质成纤维细胞的激活和纤维化。
Am J Physiol Renal Physiol. 2020 Feb 1;318(2):F375-F387. doi: 10.1152/ajprenal.00487.2019. Epub 2019 Dec 9.
10
Blocking the histone lysine 79 methyltransferase DOT1L alleviates renal fibrosis through inhibition of renal fibroblast activation and epithelial-mesenchymal transition.阻断组蛋白赖氨酸 79 甲基转移酶 DOT1L 通过抑制肾成纤维细胞激活和上皮-间充质转化减轻肾纤维化。
FASEB J. 2019 Nov;33(11):11941-11958. doi: 10.1096/fj.201801861R. Epub 2019 Aug 2.