Inflammation in atherosclerosis: pathophysiology and mechanisms.

IF 8.1 1区 生物学 Q1 CELL BIOLOGY Cell Death & Disease Pub Date : 2024-11-11 DOI:10.1038/s41419-024-07166-8
Amir Ajoolabady, Domenico Pratico, Ling Lin, Christos S Mantzoros, Suhad Bahijri, Jaakko Tuomilehto, Jun Ren
{"title":"Inflammation in atherosclerosis: pathophysiology and mechanisms.","authors":"Amir Ajoolabady, Domenico Pratico, Ling Lin, Christos S Mantzoros, Suhad Bahijri, Jaakko Tuomilehto, Jun Ren","doi":"10.1038/s41419-024-07166-8","DOIUrl":null,"url":null,"abstract":"<p><p>Atherosclerosis imposes a heavy burden on cardiovascular health due to its indispensable role in the pathogenesis of cardiovascular disease (CVD) such as coronary artery disease and heart failure. Ample clinical and experimental evidence has corroborated the vital role of inflammation in the pathophysiology of atherosclerosis. Hence, the demand for preclinical research into atherosclerotic inflammation is on the horizon. Indeed, the acquisition of an in-depth knowledge of the molecular and cellular mechanisms of inflammation in atherosclerosis should allow us to identify novel therapeutic targets with translational merits. In this review, we aimed to critically discuss and speculate on the recently identified molecular and cellular mechanisms of inflammation in atherosclerosis. Moreover, we delineated various signaling cascades and proinflammatory responses in macrophages and other leukocytes that promote plaque inflammation and atherosclerosis. In the end, we highlighted potential therapeutic targets, the pros and cons of current interventions, as well as anti-inflammatory and atheroprotective mechanisms.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"15 11","pages":"817"},"PeriodicalIF":8.1000,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11555284/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Death & Disease","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1038/s41419-024-07166-8","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Atherosclerosis imposes a heavy burden on cardiovascular health due to its indispensable role in the pathogenesis of cardiovascular disease (CVD) such as coronary artery disease and heart failure. Ample clinical and experimental evidence has corroborated the vital role of inflammation in the pathophysiology of atherosclerosis. Hence, the demand for preclinical research into atherosclerotic inflammation is on the horizon. Indeed, the acquisition of an in-depth knowledge of the molecular and cellular mechanisms of inflammation in atherosclerosis should allow us to identify novel therapeutic targets with translational merits. In this review, we aimed to critically discuss and speculate on the recently identified molecular and cellular mechanisms of inflammation in atherosclerosis. Moreover, we delineated various signaling cascades and proinflammatory responses in macrophages and other leukocytes that promote plaque inflammation and atherosclerosis. In the end, we highlighted potential therapeutic targets, the pros and cons of current interventions, as well as anti-inflammatory and atheroprotective mechanisms.

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
动脉粥样硬化中的炎症:病理生理学和机制。
动脉粥样硬化在冠心病和心力衰竭等心血管疾病(CVD)的发病机制中扮演着不可或缺的角色,给心血管健康带来了沉重负担。大量临床和实验证据证实了炎症在动脉粥样硬化病理生理学中的重要作用。因此,对动脉粥样硬化炎症的临床前研究的需求即将到来。事实上,深入了解动脉粥样硬化中炎症的分子和细胞机制,可以让我们找到具有转化价值的新型治疗靶点。在这篇综述中,我们旨在对最近发现的动脉粥样硬化的分子和细胞炎症机制进行批判性讨论和推测。此外,我们还描述了巨噬细胞和其他白细胞中促进斑块炎症和动脉粥样硬化的各种信号级联和促炎反应。最后,我们强调了潜在的治疗目标、当前干预措施的利弊以及抗炎和动脉粥样硬化保护机制。
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
Cell Death & Disease
Cell Death & Disease CELL BIOLOGY-
CiteScore
15.10
自引率
2.20%
发文量
935
审稿时长
2 months
期刊介绍: Brought to readers by the editorial team of Cell Death & Differentiation, Cell Death & Disease is an online peer-reviewed journal specializing in translational cell death research. It covers a wide range of topics in experimental and internal medicine, including cancer, immunity, neuroscience, and now cancer metabolism. Cell Death & Disease seeks to encompass the breadth of translational implications of cell death, and topics of particular concentration will include, but are not limited to, the following: Experimental medicine Cancer Immunity Internal medicine Neuroscience Cancer metabolism
期刊最新文献
RON receptor tyrosine kinase as a critical determinant in promoting tumorigenic behaviors of bladder cancer cells through regulating MMP12 and HIF-2α pathways. Advanced glycation end-products accelerate amyloid deposits in adipocyte's lipid droplets. Interaction of p53 with the Δ133p53α and Δ160p53α isoforms regulates p53 conformation and transcriptional activity. Synthetic rescue of Xeroderma Pigmentosum C phenotype via PIK3C3 downregulation. Correction: Maintenance of magnesium homeostasis by NUF2 promotes protein synthesis and anaplastic thyroid cancer progression.
×
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