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HCMV-encoded US7 and US8 act as antagonists of innate immunity by distinctively targeting TLR-signaling pathways.HCMV 编码的 US7 和 US8 通过特异地靶向 TLR 信号通路而作为先天免疫的拮抗剂。
Nat Commun. 2019 Oct 11;10(1):4670. doi: 10.1038/s41467-019-12641-4.
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Reversal of bleomycin-induced rat pulmonary fibrosis by a xenograft of human umbilical mesenchymal stem cells from Wharton's jelly.人脐带华通氏胶间充质干细胞移植逆转博莱霉素诱导的大鼠肺纤维化。
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Galectin 3 protects from cisplatin-induced acute kidney injury by promoting TLR-2-dependent activation of IDO1/Kynurenine pathway in renal DCs.半乳糖凝集素 3 通过促进 TLR-2 依赖的 IDO1/犬尿氨酸途径在肾脏 DC 中的激活来防止顺铂诱导的急性肾损伤。
Theranostics. 2019 Aug 14;9(20):5976-6001. doi: 10.7150/thno.33959. eCollection 2019.
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Metabolomics Coupled with Transcriptomics Approach Deciphering Age Relevance in Sepsis.代谢组学与转录组学方法相结合解析脓毒症中的年龄相关性
Aging Dis. 2019 Aug 1;10(4):854-870. doi: 10.14336/AD.2018.1027. eCollection 2019 Aug.
6
The Modulation of Regulatory T Cells via HMGB1/PTEN/β-Catenin Axis in LPS Induced Acute Lung Injury.高迁移率族蛋白 B1/PTEN/β-连环蛋白轴在脂多糖诱导的急性肺损伤中对调节性 T 细胞的调控作用。
Front Immunol. 2019 Jul 25;10:1612. doi: 10.3389/fimmu.2019.01612. eCollection 2019.
7
BDNF Alleviates Neuroinflammation in the Hippocampus of Type 1 Diabetic Mice via Blocking the Aberrant HMGB1/RAGE/NF-κB Pathway.脑源性神经营养因子通过阻断异常的高迁移率族蛋白B1/晚期糖基化终末产物受体/核因子κB信号通路减轻1型糖尿病小鼠海马体中的神经炎症
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8
HMGB1 promotes ductular reaction and tumorigenesis in autophagy-deficient livers.高迁移率族蛋白B1促进自噬缺陷肝脏中的小胆管反应和肿瘤发生。
J Clin Invest. 2019 May 1;129(5):2163. doi: 10.1172/JCI129233.
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J Clin Invest. 2019 Mar 4;130(4):1802. doi: 10.1172/JCI126975.

针对高迁移率族蛋白 B1 治疗脓毒症及脓毒症诱导的器官损伤。

Targeting HMGB1 for the treatment of sepsis and sepsis-induced organ injury.

机构信息

Xi'an Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Xi'an No.3 Hospital, School of Life Sciences and Medicine, Northwest University, Xi'an, 710021, China.

Department of Orthopaedics, Huaian Medical District of Jingling Hospital, Medical School of Nanjing University, Huaian, 213001, China.

出版信息

Acta Pharmacol Sin. 2022 Mar;43(3):520-528. doi: 10.1038/s41401-021-00676-7. Epub 2021 May 26.

DOI:10.1038/s41401-021-00676-7
PMID:34040166
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8888646/
Abstract

High mobility group box 1 (HMGB1) is a ubiquitous nuclear protein that is present in almost all cells and regulates the activity of innate immune responses in both intracellular and extracellular settings. Current evidence suggests that HMGB1 plays a pivotal role in human pathological and pathophysiological processes such as the inflammatory response, immune reactions, cell migration, aging, and cell death. Sepsis is a systemic inflammatory response syndrome (SIRS) that occurs in hosts in response to microbial infections with a proven or suspected infectious etiology and is the leading cause of death in intensive care units worldwide, particularly in the aging population. Dysregulated systemic inflammation is a classic characteristic of sepsis, and suppression of HMGB1 may ameliorate inflammation and improve patient outcomes. Here, we focus on the latest breakthroughs regarding the roles of HMGB1 in sepsis and sepsis-related organ injury, the ways by which HMGB1 are released, and the signaling pathways and therapeutics associated with HMGB1. This review highlights recent advances related to HMGB1: the regulation of HMBG1 might be helpful for both basic research and drug development for the treatment of sepsis and sepsis-related organ injury.

摘要

高迁移率族蛋白 B1(HMGB1)是一种普遍存在的核蛋白,几乎存在于所有细胞中,并调节细胞内和细胞外环境中固有免疫反应的活性。目前的证据表明,HMGB1 在人类病理和生理病理过程中发挥着关键作用,如炎症反应、免疫反应、细胞迁移、衰老和细胞死亡。败血症是一种全身炎症反应综合征(SIRS),发生在宿主对具有明确或可疑感染病因的微生物感染的反应中,是全球重症监护病房,特别是老龄化人群中死亡的主要原因。失调的全身炎症是败血症的一个典型特征,抑制 HMGB1 可能减轻炎症并改善患者的预后。在这里,我们重点介绍关于 HMGB1 在败血症和败血症相关器官损伤中的作用、HMGB1 释放的方式以及与 HMGB1 相关的信号通路和治疗方法的最新突破。本综述强调了与 HMGB1 相关的最新进展:HMGB1 的调节可能有助于败血症和败血症相关器官损伤的基础研究和药物开发。