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探讨硫酸乙酰肝素蛋白聚糖作为人骨髓间充质干细胞神经发生的介导物。

Exploring Heparan Sulfate Proteoglycans as Mediators of Human Mesenchymal Stem Cell Neurogenesis.

机构信息

Stem Cell and Neurogenesis Group, School of Biomedical Sciences, Genomics Research Centre, Centre for Genomics and Personalised Health, Queensland University of Technology (QUT), 60 Musk Ave, Kelvin Grove, QLD, 4059, Australia.

Max Planck Queensland Centre for the Materials Sciences of Extracellular Matrices, Kelvin Grove, Australia.

出版信息

Cell Mol Neurobiol. 2024 Mar 28;44(1):30. doi: 10.1007/s10571-024-01463-8.

Abstract

Alzheimer's disease (AD) and traumatic brain injury (TBI) are major public health issues worldwide, with over 38 million people living with AD and approximately 48 million people (27-69 million) experiencing TBI annually. Neurodegenerative conditions are characterised by the accumulation of neurotoxic amyloid beta (Aβ) and microtubule-associated protein Tau (Tau) with current treatments focused on managing symptoms rather than addressing the underlying cause. Heparan sulfate proteoglycans (HSPGs) are a diverse family of macromolecules that interact with various proteins and ligands and promote neurogenesis, a process where new neural cells are formed from stem cells. The syndecan (SDC) and glypican (GPC) HSPGs have been implicated in AD pathogenesis, acting as drivers of disease, as well as potential therapeutic targets. Human mesenchymal stem cells (hMSCs) provide an attractive therapeutic option for studying and potentially treating neurodegenerative diseases due to their relative ease of isolation and subsequent extensive in vitro expansive potential. Understanding how HSPGs regulate protein aggregation, a key feature of neurodegenerative disorders, is essential to unravelling the underlying disease processes of AD and TBI, as well as any link between these two neurological disorders. Further research may validate HSPG, specifically SDCs or GPCs, use as neurodegenerative disease targets, either via driving hMSC stem cell therapy or direct targeting.

摘要

阿尔茨海默病(AD)和创伤性脑损伤(TBI)是全球主要的公共卫生问题,全球有超过 3800 万人患有 AD,每年约有 4800 万人(27-69 岁)患有 TBI。神经退行性疾病的特征是神经毒性淀粉样β(Aβ)和微管相关蛋白 Tau(Tau)的积累,目前的治疗方法侧重于治疗症状,而不是解决根本原因。硫酸乙酰肝素蛋白聚糖(HSPGs)是一大类与各种蛋白质和配体相互作用并促进神经发生的大分子,神经发生是指从干细胞中形成新的神经细胞的过程。 syndecan(SDC)和 glypican(GPC)HSPGs 已被牵连到 AD 的发病机制中,作为疾病的驱动因素,以及潜在的治疗靶点。人骨髓间充质干细胞(hMSCs)由于其相对容易分离和随后的广泛体外扩增潜力,为研究和潜在治疗神经退行性疾病提供了有吸引力的治疗选择。了解 HSPGs 如何调节蛋白质聚集,这是神经退行性疾病的一个关键特征,对于揭示 AD 和 TBI 的潜在疾病过程以及这两种神经疾病之间的任何联系至关重要。进一步的研究可能会验证 HSPG,特别是 SDC 或 GPC,作为神经退行性疾病的靶点,无论是通过驱动 hMSC 干细胞治疗还是直接靶向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a973/11407201/36374bc21a35/10571_2024_1463_Fig1_HTML.jpg

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