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炎症反应中的抑制作用:综述

Prohibitions in the meta-inflammatory response: a review.

作者信息

Todosenko Natalia, Yurova Kristina, Vulf Maria, Khaziakhmatova Olga, Litvinova Larisa

机构信息

Center for Immunology and Cellular Biotechnology, Immanuel Kant Baltic Federal University, Kaliningrad, Russia.

Laboratory of Cellular and Microfluidic Technologies, Siberian State Medical University, Tomsk, Russia.

出版信息

Front Mol Biosci. 2024 May 15;11:1322687. doi: 10.3389/fmolb.2024.1322687. eCollection 2024.

Abstract

Prohibitins are the central regulatory element of cellular homeostasis, especially by modulating the response at different levels: Nucleus, mitochondria and membranes. Their localization and interaction with various proteins, homons, transcription and nuclear factors, and mtDNA indicate the globality and complexity of their pleiotropic properties, which remain to be investigated. A more detailed deciphering of cellular metabolism in relation to prohibitins under normal conditions and in various metabolic diseases will allow us to understand the precise role of prohibitins in the signaling cascades of PI3K/Akt, Raf/MAP/ERK, STAT3, p53, and others and to fathom their mutual influence. A valuable research perspective is to investigate the role of prohibitins in the molecular and cellular interactions between the two major players in the pathogenesis of obesity-adipocytes and macrophages - that form the basis of the meta-inflammatory response. Investigating the subtle intercellular communication and molecular cascades triggered in these cells will allow us to propose new therapeutic strategies to eliminate persistent inflammation, taking into account novel molecular genetic approaches to activate/inactivate prohibitins.

摘要

禁阻蛋白是细胞稳态的核心调节元件,特别是通过在不同水平(细胞核、线粒体和细胞膜)调节反应来实现。它们的定位以及与各种蛋白质、激素、转录因子和核因子以及线粒体DNA的相互作用表明了其多效性特性的全局性和复杂性,这些特性仍有待研究。在正常条件下以及各种代谢疾病中,更详细地解读与禁阻蛋白相关的细胞代谢,将使我们能够了解禁阻蛋白在PI3K/Akt、Raf/MAP/ERK、STAT3、p53等信号级联反应中的精确作用,并深入了解它们之间的相互影响。一个有价值的研究方向是研究禁阻蛋白在肥胖发病机制中两个主要参与者——脂肪细胞和巨噬细胞之间分子和细胞相互作用中的作用,这两者构成了代谢性炎症反应的基础。研究这些细胞中触发的微妙细胞间通讯和分子级联反应,将使我们能够提出新的治疗策略来消除持续性炎症,同时考虑到激活/失活禁阻蛋白的新分子遗传学方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8683/11133639/974e1a2c317c/fmolb-11-1322687-g001.jpg

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