Pathophysiology of Endoplasmic Reticulum Stress and the Potential Role of Dexmedetomidine as a Modulator

IF 5 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
BioFactors Pub Date : 2025-08-11 DOI:10.1002/biof.70022
Negin Karamali, Reihaneh Khaleghi Moghadam, Mohammad Borzabadi Farahani, Arman Rostamlou, Mirhamed Hoseini-Aghdam, Amirhossein Mardi, Behzad Baradaran, Leili Aghebati-Maleki
{"title":"Pathophysiology of Endoplasmic Reticulum Stress and the Potential Role of Dexmedetomidine as a Modulator","authors":"Negin Karamali,&nbsp;Reihaneh Khaleghi Moghadam,&nbsp;Mohammad Borzabadi Farahani,&nbsp;Arman Rostamlou,&nbsp;Mirhamed Hoseini-Aghdam,&nbsp;Amirhossein Mardi,&nbsp;Behzad Baradaran,&nbsp;Leili Aghebati-Maleki","doi":"10.1002/biof.70022","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>Endoplasmic reticulum (ER) stress is a fundamental process that profoundly influences immune cell function and plays a critical role in the development and progression of various physiological and pathological conditions. Understanding the underlying mechanisms of ER stress and its implications for cellular function and disease pathogenesis is of paramount importance in developing targeted therapeutic interventions. Dexmedetomidine, an alpha-2 adrenergic agonist primarily used as a sedative, has emerged as a potential modulator of ER stress. This review aims to explore the impact of Dexmedetomidine on ER stress within immune cells and its potential therapeutic implications. Dexmedetomidine exhibits the remarkable ability to inhibit the activation of ER stress pathways, preserve protein synthesis, and suppress apoptosis mediated by ER stress markers. Furthermore, Dexmedetomidine exerts regulatory effects on immune cells and inflammation by reducing the production of proinflammatory cytokines and modulating immune functions. These compelling findings suggest that Dexmedetomidine holds significant promise as a valuable therapeutic tool for conditions characterized by dysregulated ER stress and immune dysfunction.</p>\n </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 4","pages":""},"PeriodicalIF":5.0000,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"BioFactors","FirstCategoryId":"99","ListUrlMain":"https://iubmb.onlinelibrary.wiley.com/doi/10.1002/biof.70022","RegionNum":3,"RegionCategory":"生物学","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

Endoplasmic reticulum (ER) stress is a fundamental process that profoundly influences immune cell function and plays a critical role in the development and progression of various physiological and pathological conditions. Understanding the underlying mechanisms of ER stress and its implications for cellular function and disease pathogenesis is of paramount importance in developing targeted therapeutic interventions. Dexmedetomidine, an alpha-2 adrenergic agonist primarily used as a sedative, has emerged as a potential modulator of ER stress. This review aims to explore the impact of Dexmedetomidine on ER stress within immune cells and its potential therapeutic implications. Dexmedetomidine exhibits the remarkable ability to inhibit the activation of ER stress pathways, preserve protein synthesis, and suppress apoptosis mediated by ER stress markers. Furthermore, Dexmedetomidine exerts regulatory effects on immune cells and inflammation by reducing the production of proinflammatory cytokines and modulating immune functions. These compelling findings suggest that Dexmedetomidine holds significant promise as a valuable therapeutic tool for conditions characterized by dysregulated ER stress and immune dysfunction.

Abstract Image

Abstract Image

Abstract Image

内质网应激的病理生理和右美托咪定作为调节剂的潜在作用
内质网(Endoplasmic reticulum, ER)应激是深刻影响免疫细胞功能的一个基本过程,在各种生理病理状况的发生和进展中起着至关重要的作用。了解内质网应激的潜在机制及其对细胞功能和疾病发病机制的影响,对于制定有针对性的治疗干预措施至关重要。右美托咪定是一种主要用作镇静剂的α -2肾上腺素能激动剂,已成为内质网应激的潜在调节剂。本综述旨在探讨右美托咪定对免疫细胞内质网应激的影响及其潜在的治疗意义。右美托咪定具有显著的抑制内质网应激途径激活、维持蛋白合成和抑制内质网应激标志物介导的细胞凋亡的能力。此外,右美托咪定通过减少促炎细胞因子的产生和调节免疫功能,对免疫细胞和炎症有调节作用。这些令人信服的发现表明,右美托咪定作为一种有价值的治疗工具,有望治疗内质网应激失调和免疫功能障碍。
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 求助全文
来源期刊
BioFactors
BioFactors 生物-内分泌学与代谢
CiteScore
11.50
自引率
3.30%
发文量
96
审稿时长
6-12 weeks
期刊介绍: BioFactors, a journal of the International Union of Biochemistry and Molecular Biology, is devoted to the rapid publication of highly significant original research articles and reviews in experimental biology in health and disease. The word “biofactors” refers to the many compounds that regulate biological functions. Biological factors comprise many molecules produced or modified by living organisms, and present in many essential systems like the blood, the nervous or immunological systems. A non-exhaustive list of biological factors includes neurotransmitters, cytokines, chemokines, hormones, coagulation factors, transcription factors, signaling molecules, receptor ligands and many more. In the group of biofactors we can accommodate several classical molecules not synthetized in the body such as vitamins, micronutrients or essential trace elements. In keeping with this unified view of biochemistry, BioFactors publishes research dealing with the identification of new substances and the elucidation of their functions at the biophysical, biochemical, cellular and human level as well as studies revealing novel functions of already known biofactors. The journal encourages the submission of studies that use biochemistry, biophysics, cell and molecular biology and/or cell signaling approaches.
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信