炎症消退过程中的热休克反应及其在慢性退行性炎症疾病中的逐步抑制。

IF 3.3 3区 生物学 Q3 CELL BIOLOGY
Helena Trevisan Schroeder , Carlos Henrique De Lemos Muller , Thiago Gomes Heck , Mauricio Krause , Paulo Ivo Homem de Bittencourt
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引用次数: 0

摘要

热休克反应(HSR)是一种重要的生化途径,主要在蛋白毒性应激条件下协调解决炎症问题。这一过程取决于热休克转录因子-1(HSF1)对热休克蛋白(HSPs)和其他伴侣蛋白(尤其是 70kDa HSPs 家族(HSP70s))的上调。然而,在以持续低度炎症为特征的慢性退行性疾病(如胰岛素抵抗、肥胖、2 型糖尿病、非酒精性脂肪肝和心血管疾病)中,HSR 确实会逐渐受到抑制。这项研究深入探讨了这一现象背后的机制。它探讨了西方饮食和久坐不动的生活方式如何在脂肪组织细胞内最终导致内质网(ER)应激,引发一系列事件。这一系列事件包括未折叠蛋白反应(UPR)和 NLRP3 炎症小体的激活,从而导致衰老相关分泌表型(SASP)的出现和炎症在全身的传播。值得注意的是,NLRP3 炎症小体的激活不仅助长了炎症,还通过降解负责维持热休克基因启动子上 HSF1 mRNA 表达和稳定性的重要 mRNA 结合蛋白 HuR 破坏了 HSR。本文强调了理解慢性炎症如何扼杀热休克基因启动子的迫切需要,以及使用具有成本效益且易于获得的工具评估热休克基因启动子的临床意义。这种认识对于开发创新战略以预防和治疗这些慢性炎症性疾病至关重要,这些疾病继续对全球健康和福祉造成严重损失。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Heat shock response during the resolution of inflammation and its progressive suppression in chronic-degenerative inflammatory diseases

Heat shock response during the resolution of inflammation and its progressive suppression in chronic-degenerative inflammatory diseases

The heat shock response (HSR) is a crucial biochemical pathway that orchestrates the resolution of inflammation, primarily under proteotoxic stress conditions. This process hinges on the upregulation of heat shock proteins (HSPs) and other chaperones, notably the 70 kDa family of heat shock proteins, under the command of the heat shock transcription factor-1. However, in the context of chronic degenerative disorders characterized by persistent low-grade inflammation (such as insulin resistance, obesity, type 2 diabetes, nonalcoholic fatty liver disease, and cardiovascular diseases) a gradual suppression of the HSR does occur. This work delves into the mechanisms behind this phenomenon. It explores how the Western diet and sedentary lifestyle, culminating in the endoplasmic reticulum stress within adipose tissue cells, trigger a cascade of events. This cascade includes the unfolded protein response and activation of the NOD-like receptor pyrin domain-containing protein-3 inflammasome, leading to the emergence of the senescence-associated secretory phenotype and the propagation of inflammation throughout the body. Notably, the activation of the NOD-like receptor pyrin domain-containing protein-3 inflammasome not only fuels inflammation but also sabotages the HSR by degrading human antigen R, a crucial mRNA-binding protein responsible for maintaining heat shock transcription factor-1 mRNA expression and stability on heat shock gene promoters. This paper underscores the imperative need to comprehend how chronic inflammation stifles the HSR and the clinical significance of evaluating the HSR using cost-effective and accessible tools. Such understanding is pivotal in the development of innovative strategies aimed at the prevention and treatment of these chronic inflammatory ailments, which continue to take a heavy toll on global health and well-being.

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来源期刊
Cell Stress & Chaperones
Cell Stress & Chaperones 生物-细胞生物学
CiteScore
7.60
自引率
2.60%
发文量
59
审稿时长
6-12 weeks
期刊介绍: Cell Stress and Chaperones is an integrative journal that bridges the gap between laboratory model systems and natural populations. The journal captures the eclectic spirit of the cellular stress response field in a single, concentrated source of current information. Major emphasis is placed on the effects of climate change on individual species in the natural environment and their capacity to adapt. This emphasis expands our focus on stress biology and medicine by linking climate change effects to research on cellular stress responses of animals, micro-organisms and plants.
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