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[病毒感染诱导细胞衰老的机制及意义]

[Mechanism and significance of cell senescence induced by viral infection].

作者信息

Chang Yunchuang, Wu Xinna, Deng Lingli, Wang Sanying, Mao Genxiang

机构信息

College of Biological and Food Engineering, Hubei Minzu University, Enshi 445000, Hubei Province, China.

Zhejiang University School of Medicine, Hangzhou 310058, China.

出版信息

Zhejiang Da Xue Xue Bao Yi Xue Ban. 2025 Jan 25;54(1):70-80. doi: 10.3724/zdxbyxb-2024-0213.

DOI:10.3724/zdxbyxb-2024-0213
PMID:39909458
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11956860/
Abstract

Virus-induced senescence (VIS) is a significant biological phenomenon, which is associated with declining immune function, accelerating aging process and causing aging-related diseases. A variety of common viruses, including RNA viruses (such as SARS-CoV-2), DNA viruses (such as herpesviruses and hepatitis B virus), and prions can cause VIS in host cells. The primary mechanisms include abnormal activation of the cGAS-STING signaling pathway, DNA damage response, and potential correlations with the integrated stress response due to intracellular phase separation. Viral infection and cellular senescence influence each other: cellular senescence serves as a defense to restrict viral replication and transmission, while some viruses exploit cellular senescence to enhance their infectivity and replication. Understanding the mechanisms of VIS is conducive to the development of therapeutic strategies for viral infections and promotion of healthy aging. However, there is lack of research on therapeutic targets and drug development in this field so far. Although senolytics may be effective for anti-senescent cells therapy, their efficacy for VIS needs evidence from further clinical trials. This article reviews the research progress on the connection between viral infection and cellular senescence, to provide insights for the prevention and treatment of aging related diseases.

摘要

病毒诱导的衰老(VIS)是一种重要的生物学现象,它与免疫功能下降、加速衰老进程以及引发衰老相关疾病有关。多种常见病毒,包括RNA病毒(如严重急性呼吸综合征冠状病毒2)、DNA病毒(如疱疹病毒和乙型肝炎病毒)以及朊病毒,均可在宿主细胞中引发VIS。其主要机制包括cGAS-STING信号通路的异常激活、DNA损伤反应以及与由于细胞内相分离导致的综合应激反应的潜在关联。病毒感染与细胞衰老相互影响:细胞衰老作为一种防御机制,限制病毒的复制和传播,而一些病毒则利用细胞衰老来增强其传染性和复制能力。了解VIS的机制有助于开发针对病毒感染的治疗策略并促进健康衰老。然而,迄今为止,该领域在治疗靶点和药物开发方面缺乏研究。尽管衰老细胞溶解剂可能对衰老细胞治疗有效,但其对VIS的疗效尚需进一步临床试验的证据。本文综述了病毒感染与细胞衰老之间联系的研究进展,为衰老相关疾病的预防和治疗提供见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf9/11956860/9e2369db192e/1008-9292-2025-54-1-70-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf9/11956860/ee5a39f3d9cf/1008-9292-2025-54-1-70-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf9/11956860/9e2369db192e/1008-9292-2025-54-1-70-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf9/11956860/ee5a39f3d9cf/1008-9292-2025-54-1-70-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf9/11956860/9e2369db192e/1008-9292-2025-54-1-70-g002.jpg

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本文引用的文献

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ISRIB inhibits the senescence of type II pulmonary epithelial cells to alleviate pulmonary fibrosis induced by silica in mice.ISRIB 抑制 II 型肺上皮细胞衰老,减轻二氧化硅诱导的小鼠肺纤维化。
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Phase Separation: The Robust Modulator of Innate Antiviral Signaling and SARS-CoV-2 Infection.相分离:天然抗病毒信号传导和新冠病毒感染的强大调节因子
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HCMV carriage in the elderly diminishes anti-viral functionality of the adaptive immune response resulting in virus replication at peripheral sites.在老年人中,CMV 携带会降低适应性免疫反应的抗病毒功能,导致病毒在外周部位复制。
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Immune Checkpoint Molecules and Glucose Metabolism in HIV-Induced T Cell Exhaustion.HIV诱导的T细胞耗竭中的免疫检查点分子与葡萄糖代谢
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