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非编码RNA,肾结石的友还是敌?

Noncoding RNA, friend or foe for nephrolithiasis?

作者信息

Wang Qing, Yang Zhenlu, Chen Xiaolong, Yang Yuanyuan, Jiang Kehua

机构信息

Department of Urology, Guizhou Provincial People's Hospital, Guiyang, Guizhou, China.

Department of Radiology, Guizhou Provincial People's Hospital, Guiyang, Guizhou, China.

出版信息

Front Cell Dev Biol. 2024 Nov 20;12:1457319. doi: 10.3389/fcell.2024.1457319. eCollection 2024.

DOI:10.3389/fcell.2024.1457319
PMID:39633711
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11614778/
Abstract

Nephrolithiasis is one of the most common diseases in urology, characterized by notable incidence and recurrence rates, leading to significant morbidity and financial burden. Despite its prevalence, the precise mechanisms underlying stone formation remain incompletely understood, thus hindering significant advancements in kidney stone management over the past three decades. Investigating the pivotal biological molecules that govern stone formation has consistently been a challenging and high-priority task. A significant portion of mammalian genomes are transcribed into noncoding RNAs (ncRNAs), which have the ability to modulate gene expression and disease progression. They are thus emerging as a novel target class for diagnostics and pharmaceutical exploration. In recent years, the role of ncRNAs in stone formation has attracted burgeoning attention. They have been found to influence stone formation by regulating ion transportation, oxidative stress injury, inflammation, osteoblastic transformation, autophagy, and pyroptosis. These findings contributes new perspectives on the pathogenesis of nephrolithiasis. To enhance our understanding of the diagnostic and therapeutic potential of nephrolithiasis-associated ncRNAs, we summarized the expression profiles, biological functions, and clinical significance of these ncRNAs in the current review.

摘要

肾结石是泌尿外科最常见的疾病之一,其发病率和复发率都很高,会导致严重的发病率和经济负担。尽管其很常见,但结石形成的精确机制仍未完全明确,因此在过去三十年里阻碍了肾结石治疗的重大进展。研究控制结石形成的关键生物分子一直是一项具有挑战性的高优先任务。哺乳动物基因组的很大一部分被转录为非编码RNA(ncRNAs),它们能够调节基因表达和疾病进展。因此,它们正成为诊断和药物研发的一类新靶点。近年来,ncRNAs在结石形成中的作用引起了越来越多的关注。已发现它们通过调节离子转运、氧化应激损伤、炎症、成骨细胞转化、自噬和细胞焦亡来影响结石形成。这些发现为肾结石的发病机制提供了新的视角。为了加深我们对与肾结石相关的ncRNAs的诊断和治疗潜力的理解,我们在本综述中总结了这些ncRNAs的表达谱、生物学功能和临床意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58c0/11614778/3ba28c367212/fcell-12-1457319-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58c0/11614778/0ad4c2e691ad/fcell-12-1457319-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58c0/11614778/a7f571fa4ff6/fcell-12-1457319-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58c0/11614778/3ba28c367212/fcell-12-1457319-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58c0/11614778/0ad4c2e691ad/fcell-12-1457319-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58c0/11614778/a7f571fa4ff6/fcell-12-1457319-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58c0/11614778/3ba28c367212/fcell-12-1457319-g003.jpg

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本文引用的文献

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miR-148b-5p regulates hypercalciuria and calcium-containing nephrolithiasis.miR-148b-5p 调控高钙尿和含钙肾结石。
Cell Mol Life Sci. 2024 Aug 25;81(1):369. doi: 10.1007/s00018-024-05408-8.
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Metabolic Evaluation and Recurrence Prevention for Urinary Stone Patients: An EAU Guidelines Update.代谢评估和预防尿路结石患者复发:EAU 指南更新。
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Downregulating miR-184 relieves calcium oxalate crystal-mediated renal cell damage via activating the Rap1 signaling pathway.
下调miR-184通过激活Rap1信号通路减轻草酸钙晶体介导的肾细胞损伤。
Aging (Albany NY). 2023 Dec 27;15(24):14749-14763. doi: 10.18632/aging.205286.
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Exosomes from miR-23 Overexpressing Stromal Cells Suppress M1 Macrophage and Inhibit Calcium Oxalate Deposition in Hyperoxaluria Rat Model.miR-23 过表达基质细胞来源的外泌体抑制高草酸尿症大鼠模型中 M1 型巨噬细胞并抑制草酸钙沉积。
Biomed Res Int. 2023 Nov 16;2023:2883623. doi: 10.1155/2023/2883623. eCollection 2023.
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Non-coding RNAs in disease: from mechanisms to therapeutics.非编码 RNA 在疾病中的作用:从机制到治疗。
Nat Rev Genet. 2024 Mar;25(3):211-232. doi: 10.1038/s41576-023-00662-1. Epub 2023 Nov 15.
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Integrated analysis of lncRNA/circRNA-miRNA-mRNA in the proliferative phase of liver regeneration in mice with liver fibrosis.肝纤维化小鼠肝再生增殖期 lncRNA/circRNA-miRNA-mRNA 的整合分析。
BMC Genomics. 2023 Jul 24;24(1):417. doi: 10.1186/s12864-023-09478-z.
7
Acetate attenuates hyperoxaluria-induced kidney injury by inhibiting macrophage infiltration via the miR-493-3p/MIF axis.醋酸盐通过 miR-493-3p/MIF 轴抑制巨噬细胞浸润来减轻高草酸尿诱导的肾脏损伤。
Commun Biol. 2023 Mar 15;6(1):270. doi: 10.1038/s42003-023-04649-w.
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