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ZBP1驱动的严重流感中的细胞死亡。

ZBP1-driven cell death in severe influenza.

作者信息

Boyd David F, Jordan Summer Vaughn, Balachandran Siddharth

机构信息

Department of Molecular, Cell, and Developmental Biology, University of California, Santa Cruz, CA, USA.

Department of Molecular, Cell, and Developmental Biology, University of California, Santa Cruz, CA, USA.

出版信息

Trends Microbiol. 2025 May;33(5):521-532. doi: 10.1016/j.tim.2024.12.008. Epub 2025 Jan 13.

Abstract

Influenza A virus (IAV) infections can cause life-threatening illness in humans. The severity of disease is directly linked to virus replication in the alveoli of the lower respiratory tract. In particular, the lytic death of infected alveolar epithelial cells (AECs) is a major driver of influenza severity. Recent studies have begun to define the molecular mechanisms by which IAV triggers lytic cell death. Z-form nucleic-acid-binding protein 1 (ZBP1) senses replicating IAV and drives programmed cell death (PCD) in infected cells, including apoptosis and necroptosis in AECs and pyroptosis in myeloid cells. Necroptosis and pyroptosis, both lytic forms of death, contribute to pathogenesis during severe infections. Pharmacological blockade of necroptosis shows strong therapeutic potential in mouse models of lethal influenza. We suggest that targeting ZBP1-initiated necroinflammatory cell lysis, either alone or in combination antiviral drugs, will provide clinical benefit in severe influenza.

摘要

甲型流感病毒(IAV)感染可导致人类危及生命的疾病。疾病的严重程度与病毒在下呼吸道肺泡中的复制直接相关。特别是,受感染的肺泡上皮细胞(AEC)的溶解性死亡是流感严重程度的主要驱动因素。最近的研究已开始确定IAV引发溶解性细胞死亡的分子机制。Z型核酸结合蛋白1(ZBP1)感知正在复制的IAV,并驱动受感染细胞中的程序性细胞死亡(PCD),包括AEC中的细胞凋亡和坏死性凋亡以及髓样细胞中的焦亡。坏死性凋亡和焦亡都是溶解性死亡形式,在严重感染期间有助于发病机制。在致死性流感小鼠模型中,坏死性凋亡的药理学阻断显示出强大的治疗潜力。我们建议,单独或与抗病毒药物联合靶向ZBP1引发的坏死性炎症细胞裂解,将对严重流感提供临床益处。

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