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丝裂原活化蛋白激酶在药物性肾损伤中的作用。

The role of MAPK in drug-induced kidney injury.

作者信息

Cassidy Hilary, Radford Robert, Slyne Jennifer, O'Connell Sein, Slattery Craig, Ryan Michael P, McMorrow Tara

机构信息

Renal Disease Research Group, School of Biomolecular and Biomedical Sciences, UCD Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland.

出版信息

J Signal Transduct. 2012;2012:463617. doi: 10.1155/2012/463617. Epub 2012 Mar 12.

DOI:10.1155/2012/463617
PMID:22523682
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3317229/
Abstract

This paper focuses on the role that mitogen-activated protein kinases (MAPKs) play in drug-induced kidney injury. The MAPKs, of which there are four major classes (ERK, p38, JNK, and ERK5/BMK), are signalling cascades which have been found to be broadly conserved across a wide variety of organisms. MAPKs allow effective transmission of information from the cell surface to the cytosolic or nuclear compartments. Cross talk between the MAPKs themselves and with other signalling pathways allows the cell to modulate responses to a wide variety of external stimuli. The MAPKs have been shown to play key roles in both mediating and ameliorating cellular responses to stress including xenobiotic-induced toxicity. Therefore, this paper will discuss the specific role of the MAPKs in the kidney in response to injury by a variety of xenobiotics and the potential for therapeutic intervention at the level of MAPK signalling across different types of kidney disease.

摘要

本文聚焦于丝裂原活化蛋白激酶（MAPKs）在药物性肾损伤中所起的作用。MAPKs主要有四大类（细胞外信号调节激酶（ERK）、p38、应激活化蛋白激酶（JNK）和ERK5/大丝裂原活化蛋白激酶（BMK）），它们是信号级联反应，已发现其在多种生物体中广泛保守。MAPKs能使信息从细胞表面有效传递至胞质或核区室。MAPKs自身之间以及与其他信号通路之间的相互作用，使细胞能够调节对多种外部刺激的反应。MAPKs已被证明在介导和改善细胞对应激（包括外源性物质诱导的毒性）的反应中起关键作用。因此，本文将讨论MAPKs在肾脏中对各种外源性物质所致损伤的具体作用，以及在不同类型肾脏疾病中MAPK信号传导水平上进行治疗干预的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bab/3317229/27370b35e212/JST2012-463617.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bab/3317229/28ae4634e811/JST2012-463617.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bab/3317229/c677500401dd/JST2012-463617.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bab/3317229/74466010a449/JST2012-463617.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bab/3317229/acb374db03b6/JST2012-463617.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bab/3317229/27370b35e212/JST2012-463617.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bab/3317229/28ae4634e811/JST2012-463617.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bab/3317229/c677500401dd/JST2012-463617.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bab/3317229/74466010a449/JST2012-463617.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bab/3317229/acb374db03b6/JST2012-463617.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bab/3317229/27370b35e212/JST2012-463617.005.jpg

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