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p38MAPK 活性升高促进神经干细胞衰老。

Elevated p38MAPK activity promotes neural stem cell aging.

机构信息

Biodonostia Health Research Institute, Group of Cellular Oncology, San Sebastian, Spain.

Optical Spectroscopy Platform, CIC biomaGUNE, Basque Research and Technology Alliance (BRTA), San Sebastian, Spain.

出版信息

Aging (Albany NY). 2020 Apr 3;12(7):6030-6036. doi: 10.18632/aging.102994.

Abstract

Age-progressive neural stem cell (NSC) dysfunction leads to impaired neurogenesis, cognitive decline and the onset of age-related neurodegenerative pathologies. p38MAPK signalling pathway limits stem cell activity during aging in several tissues. Its role in NSCs remains controversial. In this work, we show that p38MAPK activity increases in NSCs with age in the subventricular zone (SVZ) and its pharmacological inhibition is sufficient to rejuvenate their activity . These data reveal a cell-autonomous role for p38MAPK increase in decreasing NSC homeostasis with age. This information shed light in the role of p38MAPK in NSC aging.

摘要

年龄相关的神经干细胞(NSC)功能障碍导致神经发生受损、认知能力下降和与年龄相关的神经退行性病变的发生。p38MAPK 信号通路在几种组织中限制了衰老过程中的干细胞活性。其在 NSCs 中的作用仍存在争议。在这项工作中,我们表明,在脑室下区(SVZ)中,p38MAPK 的活性随着年龄的增长而增加,其药理学抑制足以使它们的活性恢复活力。这些数据揭示了 p38MAPK 增加在随年龄降低 NSC 动态平衡中的自主作用。这些信息阐明了 p38MAPK 在 NSC 衰老中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f44/7185101/b815ced6674b/aging-12-102994-g001.jpg

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