Apelin-13可调节脂肪源性间充质干细胞改善外伤性脑损伤。

IF 2.4 3区医学 Q3 NEUROSCIENCES

Molecular and Cellular Neuroscience Pub Date : 2025-06-06 DOI:10.1016/j.mcn.2025.104016

Min Huang , Yong Zhang , Yanyang Shen, Yiqin Xu, Xuehong Liu

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引用次数: 0

摘要

创伤性脑损伤（TBI）是世界范围内最严重的神经系统疾病之一。目前，还没有有效的治疗方法。在过去的十年中，脂肪源性间充质干细胞（ADSCs）对神经元损伤的再生作用在科学界引起了相当大的关注。apelin -13是apelin家族的重要成员，具有抗凋亡、抗炎和抗氧化应激作用。ADSCs可以通过分泌调节因子来改变微环境，提高神经元的存活率。Apelin-13可以调节ADSC分化的微环境，促进ADSC的生长分化。本文将深入探讨ADSCs在脑损伤发病机制中的治疗潜力，探讨apelin-13对神经损伤的保护机制，分析apelin-13如何调控ADSCs实现对神经功能恢复的调节作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Apelin-13 can regulate adipose-derived mesenchymal stem cells to improve traumatic brain injury

Traumatic brain injury (TBI) is one of the most serious neurological diseases worldwide. At present, there is no effective treatment for TBI. The regenerative effects of adipose-derived mesenchymal stem cells (ADSCs) on neuronal injury have garnered considerable concern in the scientific community over the past decade. Apelin-13, a key member of the apelin family, has anti-apoptotic, anti-inflammatory, and antioxidative stress effects. ADSCs can modify the microenvironment to enhance neuronal survival through secreting regulatory factors. Apelin-13 can regulate the microenvironment of ADSC differentiation to promote the growth and differentiation of ADSCs. This review delves into ADSCs' therapeutic potential in brain injury pathogenesis, explores apelin-13 protective mechanism against neurological damage, and analyzes how apelin-13 regulates ADSCs to achieve the modulatory effect on neurological recovery.

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来源期刊

Molecular and Cellular Neuroscience 医学-神经科学

CiteScore

5.60

自引率

0.00%

发文量

审稿时长

37 days

期刊介绍： Molecular and Cellular Neuroscience publishes original research of high significance covering all aspects of neurosciences indicated by the broadest interpretation of the journal''s title. In particular, the journal focuses on synaptic maintenance, de- and re-organization, neuron-glia communication, and de-/regenerative neurobiology. In addition, studies using animal models of disease with translational prospects and experimental approaches with backward validation of disease signatures from human patients are welcome.