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新生脑缺氧缺血后吞噬作用介导的损伤调节。

Efferocytosis Mediated Modulation of Injury after Neonatal Brain Hypoxia-Ischemia.

机构信息

Department of Pediatrics, University of California San Francisco, San Francisco, CA 94143, USA.

Department of Neurology Weill Institute for Neurosciences, University of California San Francisco, San Francisco, CA 94143, USA.

出版信息

Cells. 2021 Apr 27;10(5):1025. doi: 10.3390/cells10051025.

Abstract

Neonatal brain hypoxia-ischemia (HI) is a leading cause of morbidity and long-term disabilities in children. While we have made significant progress in describing HI mechanisms, the limited therapies currently offered for HI treatment in the clinical setting stress the importance of discovering new targetable pathways. Efferocytosis is an immunoregulatory and homeostatic process of clearance of apoptotic cells (AC) and cellular debris, best described in the brain during neurodevelopment. The therapeutic potential of stimulating defective efferocytosis has been recognized in neurodegenerative diseases. In this review, we will explore the involvement of efferocytosis after a stroke and HI as a promising target for new HI therapies.

摘要

新生儿脑缺氧缺血(HI)是儿童发病率和长期残疾的主要原因。虽然我们在描述 HI 机制方面取得了重大进展,但目前在临床环境中提供的 HI 治疗有限的疗法强调了发现新的可靶向途径的重要性。吞噬作用是清除凋亡细胞(AC)和细胞碎片的免疫调节和体内平衡过程,在神经发育过程中在大脑中得到了最好的描述。刺激有缺陷的吞噬作用的治疗潜力已在神经退行性疾病中得到认可。在这篇综述中,我们将探讨中风和 HI 后吞噬作用的参与情况,以及作为新的 HI 治疗方法的有希望的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3487/8146813/e1fa665bbd46/cells-10-01025-g001.jpg

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