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抑制 MEG3 通过调节心力衰竭小鼠模型中 miRNA-129-5p 的表达来改善心肌细胞凋亡和自噬。

Inhibition of MEG3 ameliorates cardiomyocyte apoptosis and autophagy by regulating the expression of miRNA-129-5p in a mouse model of heart failure.

机构信息

Department of Pharmacology, College of Pharmacy, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.

Experimental Teaching Center of Public Health and Preventive Medicine, School of Public Health, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.

出版信息

Redox Rep. 2023 Dec;28(1):2224607. doi: 10.1080/13510002.2023.2224607.

DOI:10.1080/13510002.2023.2224607
PMID:37338021
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10286679/
Abstract

The long non-coding RNA, maternally expressed gene 3 (MEG3), are involved in myocardial fibrosis and compensatory hypertrophy, but its role on cardiomyocyte apoptosis and autophagy in heart failure (HF) remains unclear. The aim of this study was to investigate the effect of MEG3 on cardiomyocyte apoptosis and autophagy and the underlying mechanism. A mouse model of HF was established by subcutaneous injection of isoproterenol (ISO) for 14 days, and an in vitro oxidative stress injury model was replicated with HO for 6 h. SiRNA-MEG3 was administered in mice and in vitro cardiomyocytes to knock down MEG3 expression. Our results showed that cardiac silencing of MEG3 can significantly ameliorate ISO-induced cardiac dysfunction, hypertrophy, oxidative stress, apoptosis, excessive autophagy and fibrosis induced by ISO. In addition, inhibition of MEG3 attenuated HO-induced cardiomyocyte oxidative stress, apoptosis and autophagy in vitro. Downregulation of MEG3 significantly inhibited excessive cardiomyocyte apoptosis and autophagy induced by ISO and HO through miRNA-129-5p/ATG14/Akt signaling pathways, and reduced HO-induced cardiomyocyte apoptosis by inhibiting autophagy. In conclusion, inhibition of MEG3 ameliorates the maladaptive cardiac remodeling induced by ISO, probably by targeting the miRNA-129-5p/ATG14/Akt signaling pathway and may provide a tool for pharmaceutical intervention.

摘要

长链非编码 RNA，母系表达基因 3（MEG3）参与心肌纤维化和代偿性肥大，但它在心力衰竭（HF）中心肌细胞凋亡和自噬中的作用尚不清楚。本研究旨在探讨 MEG3 对心肌细胞凋亡和自噬的影响及其潜在机制。通过皮下注射异丙肾上腺素（ISO）14 天建立 HF 小鼠模型，并通过 6 h HO 复制体外氧化应激损伤模型。在小鼠和体外心肌细胞中给予 SiRNA-MEG3 以敲低 MEG3 表达。我们的结果表明，心脏沉默 MEG3 可显著改善 ISO 诱导的心脏功能障碍、肥大、氧化应激、凋亡、过度自噬和纤维化。此外，抑制 MEG3 可减轻 HO 诱导的体外心肌细胞氧化应激、凋亡和自噬。下调 MEG3 通过 miRNA-129-5p/ATG14/Akt 信号通路显著抑制 ISO 和 HO 诱导的心肌细胞过度凋亡和自噬，并通过抑制自噬减少 HO 诱导的心肌细胞凋亡。总之，抑制 MEG3 可改善 ISO 诱导的适应性不良性心脏重塑，可能通过靶向 miRNA-129-5p/ATG14/Akt 信号通路，并为药物干预提供工具。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/5f224731259c/YRER_A_2224607_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/1ab6c595b1b6/YRER_A_2224607_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/1d64b9ffb2ef/YRER_A_2224607_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/a9091c860df5/YRER_A_2224607_F0002_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/70851575bd3e/YRER_A_2224607_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/e11a6c40b4f0/YRER_A_2224607_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/b7276dd24f6b/YRER_A_2224607_F0005_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/6d01dd46439c/YRER_A_2224607_F0006_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/5f224731259c/YRER_A_2224607_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/1ab6c595b1b6/YRER_A_2224607_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/1d64b9ffb2ef/YRER_A_2224607_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/a9091c860df5/YRER_A_2224607_F0002_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/70851575bd3e/YRER_A_2224607_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/e11a6c40b4f0/YRER_A_2224607_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/b7276dd24f6b/YRER_A_2224607_F0005_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/6d01dd46439c/YRER_A_2224607_F0006_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b76/10286679/5f224731259c/YRER_A_2224607_F0007_OC.jpg

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引用本文的文献

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J Cardiovasc Transl Res. 2025-8-27

[2]
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Front Cell Dev Biol. 2025-7-31

[3]
LncRNA MEG3 exacerbates diabetic cardiomyopathy via activating pyroptosis signaling pathway.

Front Pharmacol. 2025-4-2

[4]
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Front Cardiovasc Med. 2025-3-20

[5]
Research progress of cPLA2 in cardiovascular diseases (Review).

Mol Med Rep. 2025-4

[6]
Regulating the regulators: long non-coding RNAs as autophagic controllers in chronic disease management.

J Biomed Sci. 2024-12-23

[7]
The function of miRNAs in the immune system's inflammatory reaction to heart failure.

Front Cardiovasc Med. 2024-12-2

[8]
Loss of Trim31 Worsens Cardiac Remodeling in a Mouse Model of Heart Failure by Enhancing the Activation of the NLRP3 Inflammasome.

Inflammation. 2024-12-13

[9]
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[10]
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本文引用的文献

[1]
Enhanced Antioxidant Effects of Naringenin Nanoparticles Synthesized using the High-Energy Ball Milling Method.

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Qi-Li-Qiang-Xin Alleviates Isoproterenol-Induced Myocardial Injury by Inhibiting Excessive Autophagy Activating AKT/mTOR Pathway.

Front Pharmacol. 2019-11-12

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