Regulation of inflammatory diseases via the control of mRNA decay.

Masanori Yoshinaga, Osamu Takeuchi
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引用次数: 0

Abstract

Inflammation orchestrates a finely balanced process crucial for microorganism elimination and tissue injury protection. A multitude of immune and non-immune cells, alongside various proinflammatory cytokines and chemokines, collectively regulate this response. Central to this regulation is post-transcriptional control, governing gene expression at the mRNA level. RNA-binding proteins such as tristetraprolin, Roquin, and the Regnase family, along with RNA modifications, intricately dictate the mRNA decay of pivotal mediators and regulators in the inflammatory response. Dysregulated activity of these factors has been implicated in numerous human inflammatory diseases, underscoring the significance of post-transcriptional regulation. The increasing focus on targeting these mechanisms presents a promising therapeutic strategy for inflammatory and autoimmune diseases. This review offers an extensive overview of post-transcriptional regulation mechanisms during inflammatory responses, delving into recent advancements, their implications in human diseases, and the strides made in therapeutic exploitation.

通过控制 mRNA 的衰变来调节炎症性疾病。
炎症是一个微妙平衡的过程,对消灭微生物和保护组织损伤至关重要。多种免疫和非免疫细胞以及各种促炎细胞因子和趋化因子共同调节着这种反应。这种调控的核心是转录后控制,即在 mRNA 水平上控制基因表达。RNA 结合蛋白(如三肽胰蛋白酶、Roquin 和 Regnase 家族)以及 RNA 修饰错综复杂地决定着炎症反应中关键介质和调节因子的 mRNA 衰减。许多人类炎症性疾病都与这些因子活性失调有关,这凸显了转录后调控的重要性。针对这些机制的研究日益受到重视,为炎症和自身免疫性疾病的治疗提供了一种前景广阔的策略。这篇综述广泛概述了炎症反应过程中的转录后调控机制,深入探讨了最新进展、它们对人类疾病的影响以及在治疗利用方面取得的进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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CiteScore
11.00
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