Cellular senescence as a potential mediator of COVID-19 severity in the elderly.,Aging Cell

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Cellular senescence as a potential mediator of COVID-19 severity in the elderly.
Aging Cell ( IF 8.0 ) Pub Date : 2020-09-21 , DOI: 10.1111/acel.13237
Jamil Nehme _{1,

2} , Michela Borghesan ₁ , Sebastian Mackedenski ₁ , Thomas G Bird _{3,

4,

5} , Marco Demaria ₁

Affiliation

SARS‐CoV‐2 is a novel betacoronavirus which infects the lower respiratory tract and can cause coronavirus disease 2019 (COVID‐19), a complex respiratory distress syndrome. Epidemiological data show that COVID‐19 has a rising mortality particularly in individuals with advanced age. Identifying a functional association between SARS‐CoV‐2 infection and the process of biological aging may provide a tractable avenue for therapy to prevent acute and long‐term disease. Here, we discuss how cellular senescence—a state of stable growth arrest characterized by pro‐inflammatory and pro‐disease functions—can hypothetically be a contributor to COVID‐19 pathogenesis, and a potential pharmaceutical target to alleviate disease severity. First, we define why older COVID‐19 patients are more likely to accumulate high levels of cellular senescence. Second, we describe how senescent cells can contribute to an uncontrolled SARS‐CoV‐2‐mediated cytokine storm and an excessive inflammatory reaction during the early phase of the disease. Third, we discuss the various mechanisms by which senescent cells promote tissue damage leading to lung failure and multi‐tissue dysfunctions. Fourth, we argue that a high senescence burst might negatively impact on vaccine efficacy. Measuring the burst of cellular senescence could hypothetically serve as a predictor of COVID‐19 severity, and targeting senescence‐associated mechanisms prior and after SARS‐CoV‐2 infection might have the potential to limit a number of severe damages and to improve the efficacy of vaccinations.

中文翻译：

细胞衰老是老年人 COVID-19 严重程度的潜在介质。

SARS-CoV-2 是一种新型 β 冠状病毒，可感染下呼吸道，并可引起 2019 年冠状病毒病 (COVID-19)，这是一种复杂的呼吸窘迫综合征。流行病学数据显示，COVID-19 的死亡率不断上升，尤其是在高龄人群中。确定 SARS-CoV-2 感染与生物衰老过程之间的功能关联可能为预防急性和长期疾病的治疗提供一条可行的途径。在这里，我们讨论细胞衰老（一种以促炎和促疾病功能为特征的稳定生长停滞状态）如何被假设为 COVID-19 发病机制的一个促成因素，以及减轻疾病严重程度的潜在药物靶标。首先，我们定义了为什么老年 COVID-19 患者更有可能积累高水平的细胞衰老。其次，我们描述了衰老细胞如何导致不受控制的 SARS-CoV-2 介导的细胞因子风暴和疾病早期阶段的过度炎症反应。第三，我们讨论衰老细胞促进组织损伤导致肺衰竭和多组织功能障碍的各种机制。第四，我们认为高衰老爆发可能会对疫苗功效产生负面影响。假设测量细胞衰老的爆发可以作为 COVID-19 严重程度的预测指标，并且针对 SARS-CoV-2 感染之前和之后的衰老相关机制可能有可能限制一些严重损害并提高治疗效果疫苗接种。

更新日期：2020-10-23

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