• 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

m A 去甲基酶 FTO 通过 YAP1 调控缺血再灌注损伤中心肌细胞的凋亡和炎症。

mA demethylase FTO regulates the apoptosis and inflammation of cardiomyocytes via YAP1 in ischemia-reperfusion injury.

机构信息

Department of Cardiology, The Affiliated Hospital of Guangdong Medical University, Zhanjiang, P.R. China.

Physical Examination Center, The Affiliated Hospital of Guangdong Medical University, Zhanjiang, P.R. China.

出版信息

Bioengineered. 2022 Mar;13(3):5443-5452. doi: 10.1080/21655979.2022.2030572.

DOI:10.1080/21655979.2022.2030572
PMID:35176940
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8974143/
Abstract

Reperfusion therapy after acute myocardial infarction can induce myocardial ischemia-reperfusion injury (IRI). Novel evidence has illustrated that N-methyladenosine (mA) modification modulates the myocardial IRI progression. Here, our study focuses on the role of mA methyltransferase fat mass and obesity-associated protein (FTO) in myocardial ischemia/reoxygenation injury and explores potential regulatory mechanisms. Results discovered that FTO down-expressed in myocardial IRI mice and hypoxia/reoxygenation (H/R)-induced cardiomyocytes. Functionally, FTO overexpression attenuated the H/R-induced apoptosis and inflammation of cardiomyocytes. Mechanistically, methylated RNA immunoprecipitation quantitative polymerase chain reaction (MeRIP-qPCR) assay and RIP assay revealed that Yap1 mRNA acted as the target of FTO in cardiomyocytes. Moreover, FTO uninstalled the methylation of Yap1 mRNA, and enforced the stability of Yap1 mRNA. Taken together, our study reveals the role of FTO in H/R-induced myocardial cell injury via mA-dependent manner, which may provide a new approach to improve myocardial IRI.

摘要

急性心肌梗死后的再灌注治疗可引起心肌缺血再灌注损伤（IRI）。新的证据表明，N6-甲基腺苷（m6A）修饰调节心肌 IRI 的进展。在这里，我们的研究集中在 m6A 甲基转移酶脂肪量和肥胖相关蛋白（FTO）在心肌缺血/再灌注损伤中的作用，并探讨其潜在的调节机制。结果发现，FTO 在心肌 IRI 小鼠和缺氧/复氧（H/R）诱导的心肌细胞中表达下调。功能上，FTO 过表达可减轻 H/R 诱导的心肌细胞凋亡和炎症。机制上，甲基化 RNA 免疫沉淀定量聚合酶链反应（MeRIP-qPCR）检测和 RIP 检测显示 Yap1 mRNA 是心肌细胞中 FTO 的靶标。此外，FTO 去除了 yap1 mRNA 的甲基化，增强了 yap1 mRNA 的稳定性。总之，我们的研究揭示了 FTO 通过 m6A 依赖的方式在 H/R 诱导的心肌细胞损伤中的作用，这可能为改善心肌 IRI 提供一种新的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f343/8974143/8288be73b30b/KBIE_A_2030572_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f343/8974143/735e9a5abbe4/KBIE_A_2030572_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f343/8974143/8ab816b3aed6/KBIE_A_2030572_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f343/8974143/ca643e7551de/KBIE_A_2030572_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f343/8974143/5291f7286259/KBIE_A_2030572_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f343/8974143/8288be73b30b/KBIE_A_2030572_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f343/8974143/735e9a5abbe4/KBIE_A_2030572_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f343/8974143/8ab816b3aed6/KBIE_A_2030572_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f343/8974143/ca643e7551de/KBIE_A_2030572_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f343/8974143/5291f7286259/KBIE_A_2030572_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f343/8974143/8288be73b30b/KBIE_A_2030572_F0005_OC.jpg

相似文献

1
mA demethylase FTO regulates the apoptosis and inflammation of cardiomyocytes via YAP1 in ischemia-reperfusion injury.m A 去甲基酶 FTO 通过 YAP1 调控缺血再灌注损伤中心肌细胞的凋亡和炎症。
Bioengineered. 2022 Mar;13(3):5443-5452. doi: 10.1080/21655979.2022.2030572.
2
METTL3 and ALKBH5 oppositely regulate mA modification of mRNA, which dictates the fate of hypoxia/reoxygenation-treated cardiomyocytes.METTL3 和 ALKBH5 对 mRNA 的 mA 修饰起相反调控作用，从而决定了低氧/复氧处理的心肌细胞的命运。
Autophagy. 2019 Aug;15(8):1419-1437. doi: 10.1080/15548627.2019.1586246. Epub 2019 Mar 17.
3
Protective mechanism of demethylase fat mass and obesity-associated protein in energy metabolism disorder of hypoxia-reoxygenation-induced cardiomyocytes.去甲基化酶脂肪量与肥胖相关蛋白在缺氧复氧诱导心肌细胞能量代谢紊乱中的保护机制
Exp Physiol. 2021 Dec;106(12):2423-2433. doi: 10.1113/EP089901. Epub 2021 Nov 21.
4
FTO-Dependent N-Methyladenosine Regulates Cardiac Function During Remodeling and Repair.FTO 依赖性 N6-甲基腺苷调节重塑和修复过程中心脏功能。
Circulation. 2019 Jan 22;139(4):518-532. doi: 10.1161/CIRCULATIONAHA.118.033794.
5
FTO overexpression inhibits apoptosis of hypoxia/reoxygenation-treated myocardial cells by regulating m6A modification of Mhrt.FTO 过表达通过调节 Mhrt 的 m6A 修饰抑制缺氧/复氧处理的心肌细胞凋亡。
Mol Cell Biochem. 2021 May;476(5):2171-2179. doi: 10.1007/s11010-021-04069-6. Epub 2021 Feb 6.
6
m6A methyltransferase WTAP regulates myocardial ischemia reperfusion injury through YTHDF1/FOXO3a signaling.m6A 甲基转移酶 WTAP 通过 YTHDF1/FOXO3a 信号通路调节心肌缺血再灌注损伤。
Apoptosis. 2023 Jun;28(5-6):830-839. doi: 10.1007/s10495-023-01818-4. Epub 2023 Mar 10.
7
WTAP-mediated mA modification of lncRNA Snhg1 improves myocardial ischemia-reperfusion injury via miR-361-5p/OPA1-dependent mitochondrial fusion.WTAP 通过介导 lncRNA Snhg1 的 mA 修饰作用改善心肌缺血再灌注损伤，其作用机制是通过 miR-361-5p/OPA1 依赖性线粒体融合。
J Transl Med. 2024 May 25;22(1):499. doi: 10.1186/s12967-024-05330-4.
8
FTO suppresses glycolysis and growth of papillary thyroid cancer via decreasing stability of APOE mRNA in an N6-methyladenosine-dependent manner.FTO 通过依赖于 N6-甲基腺苷的方式降低 APOE mRNA 的稳定性，从而抑制甲状腺乳头状癌细胞的糖酵解和生长。
J Exp Clin Cancer Res. 2022 Jan 28;41(1):42. doi: 10.1186/s13046-022-02254-z.
9
RNA N6-methyladenosine demethylase FTO promotes pancreatic cancer progression by inducing the autocrine activity of PDGFC in an mA-YTHDF2-dependent manner.RNA N6-甲基腺嘌呤去甲基酶 FTO 通过诱导 mA-YTHDF2 依赖性 PDGFC 的自分泌活性促进胰腺癌进展。
Oncogene. 2022 May;41(20):2860-2872. doi: 10.1038/s41388-022-02306-w. Epub 2022 Apr 14.
10
mA mRNA methylation controls autophagy and adipogenesis by targeting and .mA信使核糖核酸甲基化通过靶向和来控制自噬和脂肪生成。
Autophagy. 2020 Jul;16(7):1221-1235. doi: 10.1080/15548627.2019.1659617. Epub 2019 Aug 26.

引用本文的文献

1
N6-methyladenosine RNA landscape in the aged mouse hearts.衰老小鼠心脏中的N6-甲基腺嘌呤RNA图谱
Front Cardiovasc Med. 2025 Jun 18;12:1563364. doi: 10.3389/fcvm.2025.1563364. eCollection 2025.
2
Novel Insights into the Regulatory Role of N6-Methyladenosine in the Pathogenesis and Clinical Treatment of Osteoarthritis: Research Status and Prospect.N6-甲基腺苷在骨关节炎发病机制及临床治疗中调节作用的新见解：研究现状与展望
J Inflamm Res. 2025 May 27;18:6749-6766. doi: 10.2147/JIR.S508973. eCollection 2025.
3
The effects of YAP/TAZ in cardiomyocytes: a scoping review.

本文引用的文献

1
RNA m6A methylation regulators in ovarian cancer.卵巢癌中的RNA m6A甲基化调节因子
Cancer Cell Int. 2021 Nov 18;21(1):609. doi: 10.1186/s12935-021-02318-8.
2
Epigenetic modifications in acute myeloid leukemia: The emerging role of circular RNAs (Review).急性髓系白血病中的表观遗传修饰：环状 RNA 的新作用（综述）。
Int J Oncol. 2021 Dec;59(6). doi: 10.3892/ijo.2021.5287. Epub 2021 Nov 18.
3
m6A Modification in Non-Coding RNA: The Role in Cancer Drug Resistance.非编码RNA中的m6A修饰：在癌症耐药性中的作用
YAP/TAZ在心肌细胞中的作用：一项范围综述。
Mol Biol Rep. 2025 Apr 15;52(1):392. doi: 10.1007/s11033-025-10492-5.
4
A comprehensive review of m6 A methylation in coronary heart disease.冠心病中m6A甲基化的综合综述。
J Mol Med (Berl). 2025 Apr 10. doi: 10.1007/s00109-025-02540-1.
5
M6a demethylase FTO regulates the oxidative stress, mitochondrial biogenesis of cardiomyocytes and PGC-1a stability in myocardial ischemia-reperfusion injury.M6a去甲基化酶FTO在心肌缺血再灌注损伤中调节氧化应激、心肌细胞的线粒体生物发生以及PGC-1α的稳定性。
Redox Rep. 2025 Dec;30(1):2454892. doi: 10.1080/13510002.2025.2454892. Epub 2025 Jan 27.
6
FTO Alleviates Hepatic Ischemia-Reperfusion Injury by Regulating Apoptosis and Autophagy.FTO 通过调节凋亡和自噬减轻肝脏缺血再灌注损伤。
Gastroenterol Res Pract. 2025 Jan 6;2025:5587859. doi: 10.1155/grp/5587859. eCollection 2025.
7
FTO in health and disease.健康与疾病中的FTO
Front Cell Dev Biol. 2024 Dec 18;12:1500394. doi: 10.3389/fcell.2024.1500394. eCollection 2024.
8
N6-methyladenosine (m6A) modification in inflammation: a bibliometric analysis and literature review.炎症中的N6-甲基腺苷（m6A）修饰：文献计量分析与文献综述
PeerJ. 2024 Dec 13;12:e18645. doi: 10.7717/peerj.18645. eCollection 2024.
9
FTO suppresses cardiac fibrosis after myocardial infarction via mA-mediated epigenetic modification of EPRS.FTO 通过 mA 介导的 EPRS 表观遗传修饰抑制心肌梗死后的心脏纤维化。
Mol Med. 2024 Nov 13;30(1):213. doi: 10.1186/s10020-024-00985-7.
10
LncRNA UCA1 enhances NRF2 expression through the mA pathway to mitigate oxidative stress and ferroptosis in aging cardiomyocytes.长链非编码RNA UCA1通过mA途径增强NRF2表达，以减轻衰老心肌细胞中的氧化应激和铁死亡。
J Bioenerg Biomembr. 2024 Dec;56(6):607-617. doi: 10.1007/s10863-024-10045-8. Epub 2024 Nov 14.
Front Oncol. 2021 Oct 20;11:746789. doi: 10.3389/fonc.2021.746789. eCollection 2021.
4
N6-Methyladenosine-Sculpted Regulatory Landscape of Noncoding RNA.N6-甲基腺苷塑造的非编码RNA调控景观
Front Oncol. 2021 Oct 15;11:743990. doi: 10.3389/fonc.2021.743990. eCollection 2021.
5
Targeting the RNA demethylase FTO for cancer therapy.以RNA去甲基化酶FTO为靶点进行癌症治疗。
RSC Chem Biol. 2021 Jul 26;2(5):1352-1369. doi: 10.1039/d1cb00075f. eCollection 2021 Oct 7.
6
METTL14 promotes doxorubicin-induced cardiomyocyte ferroptosis by regulating the KCNQ1OT1-miR-7-5p-TFRC axis.METTL14 通过调控 KCNQ1OT1/miR-7-5p/TFRC 轴促进阿霉素诱导的心肌细胞铁死亡。
Cell Biol Toxicol. 2023 Jun;39(3):1015-1035. doi: 10.1007/s10565-021-09660-7. Epub 2021 Oct 14.
7
Crosstalk between N6-methyladenosine modification and circular RNAs: current understanding and future directions.N6-甲基腺苷修饰与环状 RNA 之间的串扰：当前的认识和未来方向。
Mol Cancer. 2021 Sep 24;20(1):121. doi: 10.1186/s12943-021-01415-6.
8
Roles of N6-Methyladenosine Demethylase FTO in Malignant Tumors Progression.N6-甲基腺苷去甲基化酶FTO在恶性肿瘤进展中的作用
Onco Targets Ther. 2021 Sep 16;14:4837-4846. doi: 10.2147/OTT.S329232. eCollection 2021.
9
FTO overexpression inhibits apoptosis of hypoxia/reoxygenation-treated myocardial cells by regulating m6A modification of Mhrt.FTO 过表达通过调节 Mhrt 的 m6A 修饰抑制缺氧/复氧处理的心肌细胞凋亡。
Mol Cell Biochem. 2021 May;476(5):2171-2179. doi: 10.1007/s11010-021-04069-6. Epub 2021 Feb 6.
10
Chronic remote ischemic conditioning for cardiovascular protection.用于心血管保护的慢性远隔缺血预处理
Cond Med. 2019 Aug;2(4):164-169.