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受损的线粒体是否会加重 SARS-CoV-2 的严重程度和致死率?

Do compromised mitochondria aggravate severity and fatality by SARS-CoV-2?

机构信息

Dr. D.Y. Patil Biotechnology & Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Cancer and Translational Research Lab, Pune, Maharashtra, India.

Department of Oral Pathology and Microbiology, Dr. D.Y. Patil Dental College and Hospital, Pune, India.

出版信息

Curr Med Res Opin. 2022 Jun;38(6):911-916. doi: 10.1080/03007995.2022.2065140. Epub 2022 Apr 22.

Abstract

At global level, the pandemic coronavirus disease 2019 (COVID-19) is known to be caused by an etiologic agent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Numerous evidence and propositions have emerged on the molecular and cellular attributes that cause COVID-19. Notwithstanding, still several key questions with reference to molecular aspects of severity of infection by SARS-CoV-2 need to be answered. In the same line, the role of healthy mitochondria to maintain intracellular temperature and their association with the severity of SARS-CoV-2 is completely missing. In this direction, preclinical and clinical data on the comorbidities in the case of mitochondrial defective disease and COVID-19 are not available. The authors propose that patients harboring primary mitochondrial disease and secondary mitochondrial dysfunction will display a higher severity and death rate compared to healthy mitochondria harboring patients.

摘要

在全球范围内,已知引起 2019 年冠状病毒病(COVID-19)的病原体是一种严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)。关于导致 COVID-19 的分子和细胞特性,已经出现了许多证据和假说。然而,关于 SARS-CoV-2 感染严重程度的分子方面,仍有几个关键问题需要解答。同样,健康线粒体在维持细胞内温度方面的作用及其与 SARS-CoV-2 严重程度的关系也完全缺失。在这方面,线粒体缺陷疾病和 COVID-19 合并症的临床前和临床数据尚不可用。作者提出,与携带健康线粒体的患者相比,携带原发性线粒体疾病和继发性线粒体功能障碍的患者的严重程度和死亡率更高。

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