Role of Mitogen Activated Protein Kinase Signaling in Parkinson's Disease

被引:124
作者
Bohush, Anastasiia [1 ]
Niewiadomska, Grazyna [1 ]
Filipek, Anna [1 ]
机构
[1] Polish Acad Sci, Nencki Inst Expt Biol, 3 Pasteur St, PL-02093 Warsaw, Poland
基金
欧盟地平线“2020”;
关键词
apoptosis; ERK1; 2; JNKs; mitochondrial dysfunction; neurodegeneration; neuro-inflammation; oxidative stress; p38; MAPKs; Parkinson's disease; ENDOPLASMIC-RETICULUM STRESS; HEME OXYGENASE-1 EXPRESSION; DOPAMINERGIC NEURONAL CELLS; AXONAL-TRANSPORT DEFECTS; LEWY BODY DISEASES; OXIDATIVE STRESS; P38; MAPK; REGULATED KINASE; MOUSE MODEL; NEURODEGENERATIVE DISEASES;
D O I
10.3390/ijms19102973
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Parkinson's disease (PD) is a neurodegenerative disorder caused by insufficient dopamine production due to the loss of 50% to 70% of dopaminergic neurons. A shortage of dopamine, which is predominantly produced by the dopaminergic neurons within the substantia nigra, causes clinical symptoms such as reduction of muscle mass, impaired body balance, akinesia, bradykinesia, tremors, postural instability, etc. Lastly, this can lead to a total loss of physical movement and death. Since no cure for PD has been developed up to now, researchers using cell cultures and animal models focus their work on searching for potential therapeutic targets in order to develop effective treatments. In recent years, genetic studies have prominently advocated for the role of improper protein phosphorylation caused by a dysfunction in kinases and/or phosphatases as an important player in progression and pathogenesis of PD. Thus, in this review, we focus on the role of selected MAP kinases such as JNKs, ERK1/2, and p38 MAP kinases in PD pathology.
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页数:17
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