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T 细胞免疫代谢与高血压中的氧化还原信号

T Cell Immunometabolism and Redox Signaling in Hypertension.

机构信息

Department of Physiology, Medical College of Georgia at Augusta University, Augusta, GA, USA.

出版信息

Curr Hypertens Rep. 2021 Dec 9;23(12):45. doi: 10.1007/s11906-021-01162-5.

Abstract

PURPOSE OF REVIEW

In this article, we summarize the current literature supporting metabolic and redox signaling pathways as important mechanisms underlying T cell activation in the context of hypertension.

RECENT FINDINGS

T cell immunometabolism undergoes dramatic remodeling in order to meet the demands of T cell activation, differentiation, and proliferation. Recent evidence demonstrates that the T cell oxidation-reduction (redox) system also undergoes significant changes upon activation, which can itself modulate metabolic processes and T cell function. Dysregulation of these signaling pathways can lead to aberrant T cell activation and inappropriate ROS production, both of which are linked to pathological conditions like hypertension. While the contribution of T cells to the progression of hypertension has been thoroughly investigated, how T cell metabolism and redox signaling changes, both separately and together, is an area of study that remains largely untouched. This review presents evidence from our own laboratory as well as others to highlight the importance of these two mechanisms in the study of hypertension.

摘要

目的综述

本文总结了目前支持代谢和氧化还原信号通路作为高血压背景下 T 细胞激活的重要机制的文献。

最近的发现

为了满足 T 细胞激活、分化和增殖的需求,T 细胞免疫代谢发生了巨大的重构。最近的证据表明,T 细胞氧化还原(redox)系统在激活时也会发生显著变化,它本身可以调节代谢过程和 T 细胞功能。这些信号通路的失调可导致异常的 T 细胞激活和不适当的 ROS 产生,这两者都与高血压等病理状况有关。虽然 T 细胞对高血压进展的贡献已经得到了深入的研究,但 T 细胞代谢和氧化还原信号的变化,无论是单独还是共同作用,都是一个研究领域,在很大程度上尚未得到探索。这篇综述从我们自己的实验室和其他实验室的证据中强调了这两个机制在高血压研究中的重要性。

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