Suppr超能文献

脓毒症免疫重塑的表观遗传机制:针对组蛋白修饰。

Epigenetic mechanisms of Immune remodeling in sepsis: targeting histone modification.

机构信息

Department of Anesthesiology, Zhongshan Hospital, Fudan University, Shanghai, China.

Shanghai Key Laboratory of Perioperative Stress and Protection, Shanghai, China.

出版信息

Cell Death Dis. 2023 Feb 11;14(2):112. doi: 10.1038/s41419-023-05656-9.

Abstract

Sepsis is a life-threatening disorder disease defined as infection-induced dysregulated immune responses and multiple organ dysfunction. The imbalance between hyperinflammation and immunosuppression is a crucial feature of sepsis immunity. Epigenetic modifications, including histone modifications, DNA methylation, chromatin remodeling, and non-coding RNA, play essential roles in regulating sepsis immunity through epi-information independent of the DNA sequence. In recent years, the mechanisms of histone modification in sepsis have received increasing attention, with ongoing discoveries of novel types of histone modifications. Due to the capacity for prolonged effects on immune cells, histone modifications can induce immune cell reprogramming and participate in the long-term immunosuppressed state of sepsis. Herein, we systematically review current mechanisms of histone modifications involved in the regulation of sepsis, summarize their role in sepsis from an immune perspective and provide potential therapeutic opportunities targeting histone modifications in sepsis treatment.

摘要

脓毒症是一种危及生命的疾病,定义为感染引起的免疫失调反应和多器官功能障碍。过度炎症反应和免疫抑制之间的失衡是脓毒症免疫的一个关键特征。表观遗传修饰,包括组蛋白修饰、DNA 甲基化、染色质重塑和非编码 RNA,通过独立于 DNA 序列的 epi 信息在调节脓毒症免疫中发挥重要作用。近年来,组蛋白修饰在脓毒症中的作用机制受到了越来越多的关注,不断发现新型的组蛋白修饰。由于对免疫细胞具有持久的影响,组蛋白修饰可以诱导免疫细胞重编程,并参与脓毒症的长期免疫抑制状态。在此,我们系统地综述了组蛋白修饰在调节脓毒症中的作用机制,从免疫角度总结了它们在脓毒症中的作用,并为针对脓毒症治疗中组蛋白修饰的潜在治疗机会提供了依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b46/9922301/06f1a0d0d598/41419_2023_5656_Fig1_HTML.jpg

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