相关实验视频

Updated: Jun 9, 2025

The Muscle Cuff Regenerative Peripheral Nerve Interface for the Amplification of Intact Peripheral Nerve Signals

The Muscle Cuff Regenerative Peripheral Nerve Interface for the Amplification of Intact Peripheral Nerve Signals

Published on: January 13, 2022

化诱导的NRG3通过ErbB4/PI3K/Akt信号通路加剧肌肉异型骨化

Lin Ma¹, Xia Kang², Jindong Tan¹

¹Department of Sports Medicine, Southwest Hospital, Army Medical University, Chongqing 400038, P.R. China.

Molecular medicine reports

|October 25, 2024

概括

周围神经损伤通过增加神经调节素3 (NRG3) 和激活纤维基原始体 (FAPs) 中的PI3K/Akt通路,使肌肉异型骨化 (HO) 恶化. 抑制这种途径为神经损伤引起的HO提供了潜在的治疗方法.

科学领域:

生物医学工程生物医学工程
再生医学是一种再生医学.
分子生物学分子生物学

背景情况:

已知外围神经损伤会恶化肌肉异型骨化 (HO).
将神经损伤与增强肌肉HO联系在一起的精确分子机制仍然不完全理解.
神经损伤后肌肉组织中细胞因子调节是研究的一个关键领域.

研究的目的:

为了研究外围神经损伤对肌肉HO发展的影响.
阐明神经受伤肌肉组织中细胞因子调节的潜在机制.
为了确定减轻神经损伤诱导的肌肉HO的潜在治疗点.

主要方法:

建立了一个小鼠模型的胃肌HO与坐骨神经损伤.
使用微计算机断层扫描,体化学染色,RNA测序,qPCR,西斑和组织阵列.
对肌肉组织衍生的纤维基原体 (FAP) 进行了体外研究.

主要成果:

坐骨神经损伤显著加剧了小鼠胃半肌肌中的HO.
神经损伤在体外增加了FAP的骨质分化.
神经调节蛋白3 (NRG3) 表达在神经损伤后增加,激活FAP中的PI3K/Akt通路并促进骨质生成.
抑制PI3K/Akt路径降低了FAP骨质原体的分化,并防止了体内HO.

结论:

周围神经损伤通过增加NRG3分泌和随后在FAP中激活PI3K/Akt通路而加剧肌肉HO.
NRG3-ErbB4-PI3K/Akt信号轴是神经损伤引起的FAP骨质性分化的关键调解器.
准PI3K/Akt路径为外围神经损伤诱导的肌肉HO提供了一个有希望的治疗策略.

关键词:

骨头改造骨头改造骨头改造细胞因子细胞因子不同类型的骨化异型化.肌肉肌肉肌肉肌肉肌肉信号传导的信号传导.

更多相关视频

Author Spotlight: Exploring Orofacial Muscle Regeneration – Insights and Innovations

Author Spotlight: Exploring Orofacial Muscle Regeneration – Insights and Innovations

Published on: December 29, 2023

Author Spotlight: Genetically Engineered Mouse Models and Pathological Characterization of Neurofibromatosis Type 1 Associated Tumors

Author Spotlight: Genetically Engineered Mouse Models and Pathological Characterization of Neurofibromatosis Type 1 Associated Tumors

Published on: May 17, 2024

相关概念视频

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...

Enzyme-linked Receptors

Enzyme-linked Receptors

Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...

Transducer Mechanism: Enzyme-Linked Receptors

Transducer Mechanism: Enzyme-Linked Receptors

Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include: