靶向 miR-199a 可减轻肥厚型心肌病中的纤维化。 - Suppr

Targeting miR-199a reduces fibrosis in hypertrophic cardiomyopathy.

作者信息

Jankauskas Stanislovas S, Varzideh Fahimeh, Kansakar Urna, Santulli Gaetano

机构信息

Department of Medicine, Division of Cardiology, Wilf Family Cardiovascular Research Institute, Einstein Institute for Neuroimmunology and Inflammation (INI), Albert Einstein College of Medicine, Montefiore University Hospital, New York, NY 10461, USA.

Department of Molecular Pharmacology, Einstein-Mount Sinai Diabetes Research Center (ES-DRC), Fleischer Institute for Diabetes and Metabolism (FIDAM), Einstein Institute for Aging Research, Albert Einstein College of Medicine, Montefiore University Hospital, New York, NY 10461, USA.

出版信息

J Mol Cell Cardiol Plus. 2023 Dec 9;7:100057. doi: 10.1016/j.jmccpl.2023.100057. eCollection 2024 Mar.

DOI:10.1016/j.jmccpl.2023.100057

PMID:39802443

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11708307/

Abstract

摘要

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcd9/11708307/db7f2a942eeb/gr1.jpg

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Targeting miR-199a reduces fibrosis in hypertrophic cardiomyopathy.靶向 miR-199a 可减轻肥厚型心肌病中的纤维化。

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Inhibition of miR-199a-3p in a murine hypertrophic cardiomyopathy (HCM) model attenuates fibrotic remodeling.在小鼠肥厚型心肌病（HCM）模型中抑制miR-199a-3p可减轻纤维化重塑。

J Mol Cell Cardiol Plus. 2023 Dec;6:100056. doi: 10.1016/j.jmccpl.2023.100056.

Circulating miR-29a, among other up-regulated microRNAs, is the only biomarker for both hypertrophy and fibrosis in patients with hypertrophic cardiomyopathy.循环 miR-29a 是肥厚型心肌病患者心肌肥厚和纤维化的唯一生物标志物，其他上调的 microRNAs 也是如此。

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Circulating Levels of MicroRNAs in Hypertrophic Cardiomyopathy: The Relationship With Left Ventricular Hypertrophy, Left Atrial Dilatation and Ventricular Depolarisation-Repolarisation Parameters.循环 microRNAs 在肥厚型心肌病中的水平：与左心室肥厚、左心房扩张和心室去极化-复极化参数的关系。

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Diverging targets mediate the pathological roleof miR-199a-5p and miR-199a-3p by promoting cardiac hypertrophy and fibrosis.不同的靶标通过促进心肌肥大和纤维化介导miR-199a-5p和miR-199a-3p的病理作用。

Mol Ther Nucleic Acids. 2021 Oct 20;26:1035-1050. doi: 10.1016/j.omtn.2021.10.013. eCollection 2021 Dec 3.

[MicroRNA-199a-3p enhances expressions of fibrosis-associated genes through targeting Smad1 in mouse cardiac fibroblasts].[微小RNA-199a-3p通过靶向小鼠心脏成纤维细胞中的Smad1增强纤维化相关基因的表达]

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MicroRNA miR-199a-3p alleviates liver fibrosis by targeting CDK17 in activated hepatic stellate cells.微小 RNA miR-199a-3p 通过靶向激活的肝星状细胞中的 CDK17 缓解肝纤维化。

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Bioinformatics prediction and experimental verification of a novel microRNA for myocardial fibrosis after myocardial infarction in rats.大鼠心肌梗死后心肌纤维化的新型 microRNA 的生物信息学预测和实验验证。

PeerJ. 2023 Feb 9;11:e14851. doi: 10.7717/peerj.14851. eCollection 2023.

microRNA-199a downregulation alleviates hyperuricemic nephropathy the PPARγ/β-catenin axis.miR-199a 下调可减轻高尿酸血症肾病中 PPARγ/β- 连环蛋白轴的作用。

J Recept Signal Transduct Res. 2022 Aug;42(4):373-381. doi: 10.1080/10799893.2021.1967392. Epub 2021 Aug 25.

Twist1-induced miR-199a-3p promotes liver fibrosis by suppressing caveolin-2 and activating TGF-β pathway. Twist1 诱导的 miR-199a-3p 通过抑制窖蛋白-2 并激活 TGF-β 通路促进肝纤维化。

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本文引用的文献

Inhibition of miR-199a-3p in a murine hypertrophic cardiomyopathy (HCM) model attenuates fibrotic remodeling.在小鼠肥厚型心肌病（HCM）模型中抑制miR-199a-3p可减轻纤维化重塑。

J Mol Cell Cardiol Plus. 2023 Dec;6:100056. doi: 10.1016/j.jmccpl.2023.100056.

LncRNA SNHG1 upregulates FANCD2 and G6PD to suppress ferroptosis by sponging miR-199a-5p/3p in hepatocellular carcinoma.长链非编码 RNA SNHG1 通过海绵吸附 miR-199a-5p/3p 上调 FANCD2 和 G6PD 来抑制肝细胞癌中的铁死亡。

Drug Discov Ther. 2023 Sep 15;17(4):248-256. doi: 10.5582/ddt.2023.01035. Epub 2023 Aug 19.

Defective extracellular matrix remodeling in brown adipose tissue is associated with fibro-inflammation and reduced diet-induced thermogenesis.棕色脂肪组织细胞外基质重塑缺陷与纤维炎症和饮食引起的产热减少有关。

Cell Rep. 2023 Jun 27;42(6):112640. doi: 10.1016/j.celrep.2023.112640. Epub 2023 Jun 13.

How common is hypertrophic cardiomyopathy… really?: Disease prevalence revisited 27 years after CARDIA.肥厚型心肌病的发病率有多高……到底有多高？：在 CARDIA 研究 27 年后重新探讨疾病的患病率。

Int J Cardiol. 2023 Jul 1;382:64-67. doi: 10.1016/j.ijcard.2023.04.005. Epub 2023 Apr 5.

miR-199a Is Upregulated in GDM Targeting the MeCP2-Trpc3 Pathway.miR-199a 在 GDM 中上调，靶向 MeCP2-Trpc3 通路。

Front Endocrinol (Lausanne). 2022 Jul 14;13:917386. doi: 10.3389/fendo.2022.917386. eCollection 2022.

Exosomes derived from bone mesenchymal stem cells attenuate myocardial fibrosis both in vivo and in vitro via autophagy activation: the key role of miR-199a-3p/mTOR pathway.骨间充质干细胞来源的外泌体通过自噬激活减轻体内外心肌纤维化：miR-199a-3p/mTOR 通路的关键作用。

Hum Cell. 2022 May;35(3):817-835. doi: 10.1007/s13577-022-00680-x. Epub 2022 Feb 21.

Diagnosis and Evaluation of Hypertrophic Cardiomyopathy: JACC State-of-the-Art Review.肥厚型心肌病的诊断与评估：美国心脏病学会心血管造影与介入学会最新临床综述

J Am Coll Cardiol. 2022 Feb 1;79(4):372-389. doi: 10.1016/j.jacc.2021.12.002.

Molecular Genetic Basis of Hypertrophic Cardiomyopathy.肥厚型心肌病的分子遗传学基础。

Circ Res. 2021 May 14;128(10):1533-1553. doi: 10.1161/CIRCRESAHA.121.318346. Epub 2021 May 13.

Adeno-associated virus-mediated delivery of anti-miR-199a tough decoys attenuates cardiac hypertrophy by targeting .腺相关病毒介导的抗miR-199a强力诱饵的递送通过靶向……减轻心肌肥大。

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The Suppression of miR-199a-3p by Promoter Methylation Contributes to Papillary Thyroid Carcinoma Aggressiveness by Targeting RAP2a and DNMT3a.启动子甲基化对miR-199a-3p的抑制作用通过靶向RAP2a和DNMT3a促进甲状腺乳头状癌的侵袭性。

Front Cell Dev Biol. 2020 Dec 7;8:594528. doi: 10.3389/fcell.2020.594528. eCollection 2020.

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Targeting miR-199a reduces fibrosis in hypertrophic cardiomyopathy.

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