The emerging role of Hippo signaling in neurodegeneration

被引:56
|
作者
Sahu, Manas Ranjan [1 ]
Mondal, Amal Chandra [1 ]
机构
[1] Jawaharlal Nehru Univ, Lab Cellular & Mol Neurobiol, Sch Life Sci, New Delhi 110067, India
关键词
apoptosis; Hippo signaling; MST; neurodegeneration; YAP/TAZ; YES-ASSOCIATED PROTEIN; PROGRAMMED CELL-DEATH; AMPK-MEDIATED REGULATION; STERILE 20-LIKE KINASES; TUMOR-SUPPRESSOR; TISSUE HOMEOSTASIS; OXIDATIVE-STRESS; REGULATE GROWTH; DROSOPHILA LATS; MST2; PATHWAY;
D O I
10.1002/jnr.24551
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Neurodegeneration refers to the complex process of progressive degeneration or neuronal apoptosis leading to a set of incurable and debilitating conditions. Physiologically, apoptosis is important in proper growth and development. However, aberrant and unrestricted apoptosis can lead to a variety of degenerative conditions including neurodegenerative diseases. Although dysregulated apoptosis has been implicated in various neurodegenerative disorders, the triggers and molecular mechanisms underlying such untimely and faulty apoptosis are still unknown. Hippo signaling pathway is one such apoptosis-regulating mechanism that has remained evolutionarily conserved from Drosophila to mammals. This pathway has gained a lot of attention for its tumor-suppressing task, but recent studies have emphasized the soaring role of this pathway in inflaming neurodegeneration. In addition, strategies promoting inactivation of this pathway have aided in the rescue of neurons from anomalous apoptosis. So, a thorough understanding of the relationship between the Hippo pathway and neurodegeneration may serve as a guide for the development of therapy for various degenerative diseases. The current review focuses on the mechanism of the Hippo signaling pathway, its upstream and downstream regulatory molecules, and its role in the genesis of numerous neurodegenerative diseases. The recent efforts employing the Hippo pathway components as targets for checking neurodegeneration have also been highlighted.
引用
收藏
页码:796 / 814
页数:19
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