神经肌肉疾病纤维化驱动:结缔组织生长因子(CCN2/CTGF)的作用与调控

Q1 Medicine
Daniela L. Rebolledo , Kenneth E. Lipson , Enrique Brandan
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引用次数: 16

摘要

结缔组织生长因子或细胞通信网络2 (CCN2/CTGF)是CCN家族的一种基质细胞蛋白,参与几个关键的生物学过程。在骨骼肌中,CCN2/CTGF丰度在多种神经肌肉病变(包括肌肉营养不良、神经退行性疾病、肌肉去神经支配和肌肉过度使用)的人体肌肉活检和/或动物模型中升高。在这种情况下,CCN2/CTGF深度参与细胞外基质(ECM)调节,作为一种强促纤维化因子,促进过度的ECM积累。病理状态下降低CCN2/CTGF水平或生物活性可减少纤维化,改善肌肉结构和功能。在这项工作中,我们总结了CCN2/CTGF在与神经肌肉病变相关的纤维化中的作用,以及在骨骼肌中调节其表达的机制和信号通路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Driving fibrosis in neuromuscular diseases: Role and regulation of Connective tissue growth factor (CCN2/CTGF)

Driving fibrosis in neuromuscular diseases: Role and regulation of Connective tissue growth factor (CCN2/CTGF)

Driving fibrosis in neuromuscular diseases: Role and regulation of Connective tissue growth factor (CCN2/CTGF)

Connective tissue growth factor or cellular communication network 2 (CCN2/CTGF) is a matricellular protein member of the CCN family involved in several crucial biological processes. In skeletal muscle, CCN2/CTGF abundance is elevated in human muscle biopsies and/or animal models for diverse neuromuscular pathologies, including muscular dystrophies, neurodegenerative disorders, muscle denervation, and muscle overuse. In this context, CCN2/CTGF is deeply involved in extracellular matrix (ECM) modulation, acting as a strong pro-fibrotic factor that promotes excessive ECM accumulation. Reducing CCN2/CTGF levels or biological activity in pathological conditions can decrease fibrosis, improve muscle architecture and function. In this work, we summarize information about the role of CCN2/CTGF in fibrosis associated with neuromuscular pathologies and the mechanisms and signaling pathways that regulate their expression in skeletal muscle.

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来源期刊
Matrix Biology Plus
Matrix Biology Plus Medicine-Histology
CiteScore
9.00
自引率
0.00%
发文量
25
审稿时长
105 days
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