缺血性脑卒中后纤维化瘢痕形成:靶向Sonic hedgehog信号通路减少瘢痕

IF 5.9 2区 医学 Q2 CELL BIOLOGY
Neural Regeneration Research Pub Date : 2026-02-01 Epub Date: 2025-02-24 DOI:10.4103/NRR.NRR-D-24-00999
Jun Wen, Hao Tang, Mingfen Tian, Ling Wang, Qinghuan Yang, Yong Zhao, Xuemei Li, Yu Ren, Jiani Wang, Li Zhou, Yongjun Tan, Haiyun Wu, Xinrui Cai, Yilin Wang, Hui Cao, Jianfeng Xu, Qin Yang
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引用次数: 0

摘要

摘要:最近的研究表明,脑缺血损伤后纤维化瘢痕的形成因微环境的不同而产生不同的影响。然而,人们对脑缺血损伤后纤维化是如何诱导和调节的知之甚少。音速刺猬信号参与了心脏、肝脏、肺和肾脏的纤维化。Shh信号是否调节脑缺血卒中后纤维化瘢痕的形成及其内在机制尚不清楚。在这项研究中,我们发现在急性缺血性脑卒中患者和大脑中动脉闭塞/再灌注损伤大鼠模型中,Sonic Hedgehog 的表达上调。在大脑中动脉闭塞大鼠模型和转化生长因子-β1诱导的体外纤维化细胞模型中,Sonic hedgehog和Mitofusin 2的表达均有所增加。激活Sonic hedgehog信号通路可增强磷酸化Smad 3和Mitofusin 2蛋白的表达,促进纤维化疤痕的形成,保护突触或促进突触发生,缓解大脑中动脉闭塞/再灌注损伤后的神经功能缺损,减少细胞凋亡,促进脑膜成纤维细胞向肌成纤维细胞转化,增强脑膜成纤维细胞的增殖和迁移。Smad3 磷酸化抑制剂 SIS3 逆转了音速刺猬信号通路激活所诱导的效应。生物信息学分析显示,Sonic hedgehog与Smad3之间、Sonic hedgehog与Mitofusin 2之间以及Smad3与Mitofusin 2之间存在显著相关性。 这些发现表明,Sonic hedgehog信号通路可能通过调节Smad3磷酸化来影响Mitofusin 2的表达,从而调节缺血性脑卒中后早期纤维化疤痕的形成并影响预后。Sonic Hedgehog 信号通路可作为脑卒中治疗的新靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Fibrotic scar formation after cerebral ischemic stroke: Targeting the Sonic hedgehog signaling pathway for scar reduction.

JOURNAL/nrgr/04.03/01300535-202602000-00044/figure1/v/2025-05-05T160104Z/r/image-tiff Recent studies have shown that fibrotic scar formation following cerebral ischemic injury has varying effects depending on the microenvironment. However, little is known about how fibrosis is induced and regulated after cerebral ischemic injury. Sonic hedgehog signaling participates in fibrosis in the heart, liver, lung, and kidney. Whether Shh signaling modulates fibrotic scar formation after cerebral ischemic stroke and the underlying mechanisms are unclear. In this study, we found that Sonic Hedgehog expression was upregulated in patients with acute ischemic stroke and in a middle cerebral artery occlusion/reperfusion injury rat model. Both Sonic hedgehog and Mitofusin 2 showed increased expression in the middle cerebral artery occlusion rat model and in vitro fibrosis cell model induced by transforming growth factor-beta 1. Activation of the Sonic hedgehog signaling pathway enhanced the expression of phosphorylated Smad 3 and Mitofusin 2 proteins, promoted the formation of fibrotic scars, protected synapses or promoted synaptogenesis, alleviated neurological deficits following middle cerebral artery occlusion/reperfusion injury, reduced cell apoptosis, facilitated the transformation of meninges fibroblasts into myofibroblasts, and enhanced the proliferation and migration of meninges fibroblasts. The Smad3 phosphorylation inhibitor SIS3 reversed the effects induced by Sonic hedgehog signaling pathway activation. Bioinformatics analysis revealed significant correlations between Sonic hedgehog and Smad3, between Sonic hedgehog and Mitofusin 2, and between Smad3 and Mitofusin 2. These findings suggest that Sonic hedgehog signaling may influence Mitofusin 2 expression by regulating Smad3 phosphorylation, thereby modulating the formation of early fibrotic scars following cerebral ischemic stroke and affecting prognosis. The Sonic Hedgehog signaling pathway may serve as a new therapeutic target for stroke treatment.

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来源期刊
Neural Regeneration Research
Neural Regeneration Research CELL BIOLOGY-NEUROSCIENCES
CiteScore
8.00
自引率
9.80%
发文量
515
审稿时长
1.0 months
期刊介绍: Neural Regeneration Research (NRR) is the Open Access journal specializing in neural regeneration and indexed by SCI-E and PubMed. The journal is committed to publishing articles on basic pathobiology of injury, repair and protection to the nervous system, while considering preclinical and clinical trials targeted at improving traumatically injuried patients and patients with neurodegenerative diseases.
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