胚芽基质出血的发病机制:单细胞转录组学的启示。

Jiapei Chen,Jennifer Ja-Yoon Choi,Pin-Yeh Lin,Eric J Huang
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引用次数: 0

摘要

胚芽基质蕴藏着产前人脑表皮下的神经源龛,可产生丰富的 GABA 能神经元。在早产儿中,胚芽基质特别容易发生出血,从而破坏神经发生并导致严重的神经发育后遗症。然而,促进胚芽基质出血的疾病机制仍不清楚。在此,我们回顾了利用单细胞转录组学揭示支配产前人脑生发基质中神经发生和血管生成的新机制的最新进展。这些方法还揭示了免疫-血管相互作用在促进胚芽基质中血管形态发生方面的关键作用,以及活化的中性粒细胞和单核细胞产生的促炎因子如何破坏这一过程并导致出血。这些结果共同揭示了胚芽基质出血的基本疾病机制和治疗干预措施。
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Pathogenesis of Germinal Matrix Hemorrhage: Insights from Single-Cell Transcriptomics.
The germinal matrix harbors neurogenic niches in the subpallium of the prenatal human brain that produce abundant GABAergic neurons. In preterm infants, the germinal matrix is particularly vulnerable to developing hemorrhage, which disrupts neurogenesis and causes severe neurodevelopmental sequelae. However, the disease mechanisms that promote germinal matrix hemorrhage remain unclear. Here, we review recent advances using single-cell transcriptomics to uncover novel mechanisms that govern neurogenesis and angiogenesis in the germinal matrix of the prenatal human brain. These approaches also reveal the critical role of immune-vascular interaction that promotes vascular morphogenesis in the germinal matrix and how proinflammatory factors from activated neutrophils and monocytes can disrupt this process, leading to hemorrhage. Collectively, these results reveal fundamental disease mechanisms and therapeutic interventions for germinal matrix hemorrhage.
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来源期刊
CiteScore
62.60
自引率
0.00%
发文量
40
期刊介绍: The Annual Review of Pathology: Mechanisms of Disease is a scholarly journal that has been published since 2006. Its primary focus is to provide a comprehensive overview of recent advancements in our knowledge of the causes and development of significant human diseases. The journal places particular emphasis on exploring the current and evolving concepts of disease pathogenesis, as well as the molecular genetic and morphological changes associated with various diseases. Additionally, the journal addresses the clinical significance of these findings. In order to increase accessibility and promote the broad dissemination of research, the current volume of the journal has transitioned from a gated subscription model to an open access format. This change has been made possible through the Annual Reviews' Subscribe to Open program, which allows all articles published in this volume to be freely accessible to readers. As part of this transition, all articles in the journal are published under a Creative Commons Attribution (CC BY) license, which encourages open sharing and use of the research.
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