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哺乳动物金属硫蛋白-2A与氧化应激

Mammalian Metallothionein-2A and Oxidative Stress.

作者信息

Ling Xue-Bin, Wei Hong-Wei, Wang Jun, Kong Yue-Qiong, Wu Yu-You, Guo Jun-Li, Li Tian-Fa, Li Ji-Ke

机构信息

Department of Cardiovascular Institute, Affiliated Hospital of Hainan Medical College, Haikou 570102, China.

出版信息

Int J Mol Sci. 2016 Sep 6;17(9):1483. doi: 10.3390/ijms17091483.

DOI:10.3390/ijms17091483
PMID:27608012
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5037761/
Abstract

Mammalian metallothionein-2A (MT2A) has received considerable attention in recent years due to its crucial pathophysiological role in anti-oxidant, anti-apoptosis, detoxification and anti-inflammation. For many years, most studies evaluating the effects of MT2A have focused on reactive oxygen species (ROS), as second messengers that lead to oxidative stress injury of cells and tissues. Recent studies have highlighted that oxidative stress could activate mitogen-activated protein kinases (MAPKs), and MT2A, as a mediator of MAPKs, to regulate the pathogenesis of various diseases. However, the molecule mechanism of MT2A remains elusive. A deeper understanding of the functional, biochemical and molecular characteristics of MT2A would be identified, in order to bring new opportunities for oxidative stress therapy.

摘要

近年来,哺乳动物金属硫蛋白-2A(MT2A)因其在抗氧化、抗凋亡、解毒和抗炎等方面的关键病理生理作用而备受关注。多年来,大多数评估MT2A作用的研究都集中在活性氧(ROS)上,ROS作为导致细胞和组织氧化应激损伤的第二信使。最近的研究强调,氧化应激可激活丝裂原活化蛋白激酶(MAPKs),而MT2A作为MAPKs的介质,参与调节各种疾病的发病机制。然而,MT2A的分子机制仍不清楚。深入了解MT2A的功能、生化和分子特性,将为氧化应激治疗带来新的机遇。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a8/5037761/dd6b118407e7/ijms-17-01483-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a8/5037761/80d5ea672b7e/ijms-17-01483-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a8/5037761/e93367de44d7/ijms-17-01483-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a8/5037761/dd6b118407e7/ijms-17-01483-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a8/5037761/80d5ea672b7e/ijms-17-01483-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a8/5037761/e93367de44d7/ijms-17-01483-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a8/5037761/dd6b118407e7/ijms-17-01483-g003.jpg

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