Histone Deacetylases (HDACs) Roles in Inflammation-mediated Diseases; Current Knowledge.

IF 1.8 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Cell Biochemistry and Biophysics Pub Date : 2024-10-18 DOI:10.1007/s12013-024-01587-0
Saade Abdalkareem Jasim, Farag M A Altalbawy, Mohammad Abohassan, Enwa Felix Oghenemaro, Ashok Kumar Bishoyi, Ravindra Pal Singh, Parjinder Kaur, G V Sivaprasad, Jaafaru Sani Mohammed, Hanen Mahmod Hulail
{"title":"Histone Deacetylases (HDACs) Roles in Inflammation-mediated Diseases; Current Knowledge.","authors":"Saade Abdalkareem Jasim, Farag M A Altalbawy, Mohammad Abohassan, Enwa Felix Oghenemaro, Ashok Kumar Bishoyi, Ravindra Pal Singh, Parjinder Kaur, G V Sivaprasad, Jaafaru Sani Mohammed, Hanen Mahmod Hulail","doi":"10.1007/s12013-024-01587-0","DOIUrl":null,"url":null,"abstract":"<p><p>The histone acetyl transferases (HATs) and histone deacetylases (HDACs), which are mostly recognized for their involvement in regulating chromatin remodeling via histone acetylation/deacetylation, have been shown to also change several non-histone proteins to regulate other cellular processes. Acetylation affects the activity or function of cytokine receptors, nuclear hormone receptors, intracellular signaling molecules, and transcription factors in connection to inflammation. Some small-molecule HDAC inhibitors are utilized as anticancer medications in clinical settings due to their capability to regulate cellular growth arrest, differentiation, and death. Here, we summarize our present knowledge of the innate and adaptive immunological pathways that classical HDAC enzymes control. The aim is to justify the targeted (or non-targeted) use of inhibitors against certain HDAC enzymes in inflammatory diseases such as arthritis, inflammatory bowel diseases (IBD), airways inflammation and neurological diseases.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8000,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Biochemistry and Biophysics","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s12013-024-01587-0","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

The histone acetyl transferases (HATs) and histone deacetylases (HDACs), which are mostly recognized for their involvement in regulating chromatin remodeling via histone acetylation/deacetylation, have been shown to also change several non-histone proteins to regulate other cellular processes. Acetylation affects the activity or function of cytokine receptors, nuclear hormone receptors, intracellular signaling molecules, and transcription factors in connection to inflammation. Some small-molecule HDAC inhibitors are utilized as anticancer medications in clinical settings due to their capability to regulate cellular growth arrest, differentiation, and death. Here, we summarize our present knowledge of the innate and adaptive immunological pathways that classical HDAC enzymes control. The aim is to justify the targeted (or non-targeted) use of inhibitors against certain HDAC enzymes in inflammatory diseases such as arthritis, inflammatory bowel diseases (IBD), airways inflammation and neurological diseases.

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
组蛋白去乙酰化酶 (HDAC) 在炎症介导的疾病中的作用;当前知识。
组蛋白乙酰转移酶(HATs)和组蛋白去乙酰化酶(HDACs)主要通过组蛋白乙酰化/去乙酰化参与调节染色质重塑,但它们也能改变几种非组蛋白蛋白质,从而调节其他细胞过程。乙酰化会影响细胞因子受体、核激素受体、细胞内信号分子和转录因子的活性或功能,从而引发炎症。一些小分子 HDAC 抑制剂因其调节细胞生长停滞、分化和死亡的能力而被用作临床抗癌药物。在此,我们总结了目前我们对经典 HDAC 酶所控制的先天性和适应性免疫途径的了解。目的是证明在关节炎、炎症性肠病(IBD)、气道炎症和神经系统疾病等炎症性疾病中靶向(或非靶向)使用某些 HDAC 酶抑制剂的合理性。
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 Biochemistry and Biophysics
Cell Biochemistry and Biophysics 生物-生化与分子生物学
CiteScore
4.40
自引率
0.00%
发文量
72
审稿时长
7.5 months
期刊介绍: Cell Biochemistry and Biophysics (CBB) aims to publish papers on the nature of the biochemical and biophysical mechanisms underlying the structure, control and function of cellular systems The reports should be within the framework of modern biochemistry and chemistry, biophysics and cell physiology, physics and engineering, molecular and structural biology. The relationship between molecular structure and function under investigation is emphasized. Examples of subject areas that CBB publishes are: · biochemical and biophysical aspects of cell structure and function; · interactions of cells and their molecular/macromolecular constituents; · innovative developments in genetic and biomolecular engineering; · computer-based analysis of tissues, cells, cell networks, organelles, and molecular/macromolecular assemblies; · photometric, spectroscopic, microscopic, mechanical, and electrical methodologies/techniques in analytical cytology, cytometry and innovative instrument design For articles that focus on computational aspects, authors should be clear about which docking and molecular dynamics algorithms or software packages are being used as well as details on the system parameterization, simulations conditions etc. In addition, docking calculations (virtual screening, QSAR, etc.) should be validated either by experimental studies or one or more reliable theoretical cross-validation methods.
期刊最新文献
Iron Overloading Potentiates the Antitumor Activity of 5-Fluorouracil by Promoting Apoptosis and Ferroptosis in Colorectal Cancer Cells. Navigating the Fractional Calcium Dynamics of Orai Mechanism in Polar Dimensions. BAG3 Mediated Down-regulation in Expression of p66shc has Ramifications on Cellular Proliferation, Apoptosis and Metastasis. Rutin Ameliorates Inflammation and Oxidative Stress in Ulcerative Colitis by Inhibiting NLRP3 Inflammasome Signaling Pathway. Study on the Role of EPHB6 in Inhibiting the Malignant Progression of Cervical Cancer C33A Cells by Binding to CBX7.
×
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