Landay Alan, Bartley Jenna, Banerjee Dishary, Hargis Geneva, Haynes Laura, Keshavarzian Ali, Kuo Chia-Ling, Kwon Oh Sung, Li Sheng, Li Shuzhao, Oh Julia, Ozbolat Ibrahim Tarik, Ucar Duygu, Xu Ming, Yao Xudong, Unutmaz Derya, Kuchel George A
Department of Medicine, Rush School of Medicine, Chicago, IL USA.
UConn Center on Aging, University of Connecticut School of Medicine, Farmington, CT 06030, USA.
Front Aging. 2021 Jul;2. doi: 10.3389/fragi.2021.695218. Epub 2021 Jul 23.
Aging has emerged as the greatest and most prevalent risk factor for the development of severe COVID-19 infection and death following exposure to the SARS-CoV-2 virus. The presence of multiple co-existing chronic diseases and conditions of aging further enhances this risk. Biological aging not only enhances the risk of chronic diseases, but the presence of such conditions further accelerates varied biological processes or "hallmarks" implicated in aging. Given growing evidence that it is possible to slow the rate of many biological aging processes using pharmacological compounds has led to the proposal that such geroscience-guided interventions may help enhance immune resilience and improve outcomes in the face of SARS-CoV-2 infection. Our review of the literature indicates that most, if not all, hallmarks of aging may contribute to the enhanced COVID-19 vulnerability seen in frail older adults. Moreover, varied biological mechanisms implicated in aging do not function in isolation from each other, and exhibit intricate effects on each other. With all of these considerations in mind, we highlight limitations of current strategies mostly focused on individual single mechanisms, and we propose an approach which is far more multidisciplinary and systems-based emphasizing network topology of biological aging and geroscience-guided approaches to COVID-19.
衰老已成为感染严重急性呼吸综合征冠状病毒2（SARS-CoV-2）后发生重症2019冠状病毒病（COVID-19）感染和死亡的最大且最普遍的风险因素。多种并存的慢性疾病和衰老状况进一步增加了这种风险。生物衰老不仅会增加患慢性病的风险，而且这些疾病的存在还会进一步加速与衰老相关的各种生物学过程或“特征”。鉴于越来越多的证据表明，使用药物化合物有可能减缓许多生物衰老过程的速度，因此有人提出，这种以老年科学为指导的干预措施可能有助于增强免疫恢复力，并改善面对SARS-CoV-2感染时的结果。我们对文献的综述表明，衰老的大多数（如果不是全部）特征可能导致体弱老年人中COVID-19易感性增加。此外，与衰老相关的各种生物学机制并非相互独立起作用，而是相互之间表现出复杂的影响。考虑到所有这些因素，我们强调了当前主要侧重于单个单一机制的策略的局限性，并提出了一种更具多学科性和基于系统的方法，强调生物衰老的网络拓扑结构以及以老年科学为指导的COVID-19应对方法。
