TNF-alpha Is not a Miscreant: A Hero for Basal Nrf2-Antioxidant Signaling.

Reactive oxygen species (Apex, N.C.) Pub Date : 2017-09-01 DOI:10.20455/ros.2017.849

Rajasekaran Namakkal-Soorappan

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引用次数: 1

Abstract

About three decades of intensive research suggest that tumor necrosis factor-alpha (TNF-α) is a "miscreant". Although it is obvious that supra-physiological TNF-α levels are deleterious to cellular activities leading to a variety of pathological conditions, it is unlikely that complete removal of TNF-α is cytoprotective. Are we rejecting the basal physiological role of TNF-α as a reactive oxygen species (ROS) producer that is key and essential for numerous basal cell signaling processes? We believe that there are important protective roles for TNF-α under basal/physiological conditions. We propose that one such role is that of signaling through nuclear erythroid 2 p45 related factor-2/antioxidant response element (Nrf2/ARE). Confirming our hypothesis that TNF-α is necessary and sufficient for the basal activation of Nrf2/ARE transcriptional pathways, will change the existing paradigms on the function of TNF-α. This article briefly reviews the canonical role of TNF-α as miscreant and introduces a new role as a hero in the context of Nrf2-antioxidant signaling.

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tnf - α不是坏人:基础nrf2 -抗氧化信号的英雄。

近三十年的深入研究表明，肿瘤坏死因子-α (TNF-α)是一个“恶棍”。虽然很明显，超生理水平的TNF-α对细胞活动有害，导致多种病理状况，但完全去除TNF-α不太可能具有细胞保护作用。我们是否拒绝TNF-α作为活性氧(ROS)生产者的基础生理作用，这是许多基底细胞信号传导过程的关键和必需的?我们认为TNF-α在基础/生理条件下具有重要的保护作用。我们提出其中一个作用是通过核红细胞2 p45相关因子-2/抗氧化反应元件(Nrf2/ARE)进行信号传导。证实我们的假设TNF-α是Nrf2/ARE转录途径基础激活的必要和充分条件，将改变TNF-α功能的现有范式。本文简要回顾了TNF-α作为恶棍的典型作用，并介绍了nrf2 -抗氧化信号背景下TNF-α作为英雄的新作用。

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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Reactive oxygen species (Apex, N.C.)

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