Insights into RNA N6-methyladenosine and programmed cell death in atherosclerosis.

IF 6 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Molecular Medicine Pub Date : 2024-09-03 DOI:10.1186/s10020-024-00901-z
Haijiao Long, Yulu Yu, Jie Ouyang, Hongwei Lu, Guojun Zhao
{"title":"Insights into RNA N6-methyladenosine and programmed cell death in atherosclerosis.","authors":"Haijiao Long, Yulu Yu, Jie Ouyang, Hongwei Lu, Guojun Zhao","doi":"10.1186/s10020-024-00901-z","DOIUrl":null,"url":null,"abstract":"<p><p>N6-methyladenosine (m<sup>6</sup>A) modification stands out among various RNA modifications as the predominant form within eukaryotic cells, influencing numerous cellular processes implicated in disease development. m<sup>6</sup>A modification has gained increasing attention in the development of atherosclerosis and has become a research hotspot in recent years. Programmed cell death (PCD), encompassing apoptosis, autophagy, pyroptosis, ferroptosis, and necroptosis, plays a pivotal role in atherosclerosis pathogenesis. In this review, we delve into the intricate interplay between m<sup>6</sup>A modification and diverse PCD pathways, shedding light on their complex association during the onset and progression of atherosclerosis. Clarifying the relationship between m<sup>6</sup>A and PCD in atherosclerosis is of great significance to provide novel strategies for cardiovascular disease treatment.</p>","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"30 1","pages":"137"},"PeriodicalIF":6.0000,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11373444/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s10020-024-00901-z","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

N6-methyladenosine (m6A) modification stands out among various RNA modifications as the predominant form within eukaryotic cells, influencing numerous cellular processes implicated in disease development. m6A modification has gained increasing attention in the development of atherosclerosis and has become a research hotspot in recent years. Programmed cell death (PCD), encompassing apoptosis, autophagy, pyroptosis, ferroptosis, and necroptosis, plays a pivotal role in atherosclerosis pathogenesis. In this review, we delve into the intricate interplay between m6A modification and diverse PCD pathways, shedding light on their complex association during the onset and progression of atherosclerosis. Clarifying the relationship between m6A and PCD in atherosclerosis is of great significance to provide novel strategies for cardiovascular disease treatment.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
透视动脉粥样硬化中的 RNA N6-甲基腺苷和程序性细胞死亡
N6-甲基腺苷(m6A)修饰是真核细胞内各种 RNA 修饰的主要形式,影响着许多与疾病发展有关的细胞过程。m6A 修饰在动脉粥样硬化的发展过程中日益受到关注,近年来已成为研究热点。程序性细胞死亡(PCD)包括细胞凋亡、自噬、热凋亡、铁凋亡和坏死,在动脉粥样硬化发病机制中起着关键作用。在这篇综述中,我们将深入探讨 m6A 修饰与多种 PCD 途径之间错综复杂的相互作用,揭示它们在动脉粥样硬化发生和发展过程中的复杂关联。厘清动脉粥样硬化中 m6A 与 PCD 的关系对于提供治疗心血管疾病的新策略具有重要意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Molecular Medicine
Molecular Medicine 医学-生化与分子生物学
CiteScore
8.60
自引率
0.00%
发文量
137
审稿时长
1 months
期刊介绍: Molecular Medicine is an open access journal that focuses on publishing recent findings related to disease pathogenesis at the molecular or physiological level. These insights can potentially contribute to the development of specific tools for disease diagnosis, treatment, or prevention. The journal considers manuscripts that present material pertinent to the genetic, molecular, or cellular underpinnings of critical physiological or disease processes. Submissions to Molecular Medicine are expected to elucidate the broader implications of the research findings for human disease and medicine in a manner that is accessible to a wide audience.
期刊最新文献
Co-culture of human AT2 cells with fibroblasts reveals a MUC5B phenotype: insights from an organoid model. TIMP1 regulates ferroptosis in osteoblasts by inhibiting TFRC ubiquitination: an in vitro and in vivo study. Exploring Smad5: a review to pave the way for a deeper understanding of the pathobiology of common respiratory diseases. Hyperoside induces ferroptosis in chronic myeloid leukemia cells by targeting NRF2. FUT8 upregulates CD36 and its core fucosylation to accelerate pericyte-myofibroblast transition through the mitochondrial-dependent apoptosis pathway during AKI-CKD.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1