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.

中文翻译：

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生发基质出血的发病机制：来自单细胞转录组学的见解


生发基质在产前人脑的钯下隐藏着神经源性生态位，可产生丰富的 GABA 能神经元。在早产儿中，生发基质特别容易发生出血，出血会破坏神经发生并导致严重的神经发育后遗症。然而，促进生发基质出血的疾病机制仍不清楚。在这里，我们回顾了使用单细胞转录组学的最新进展，以揭示控制产前人脑生发基质中神经发生和血管生成的新机制。这些方法还揭示了免疫-血管相互作用的关键作用，它促进了生发基质中的血管形态发生，以及来自活化的中性粒细胞和单核细胞的促炎因子如何破坏这一过程，从而导致出血。总的来说，这些结果揭示了生发基质出血的基本疾病机制和治疗干预措施。