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SARS-CoV-2 加重了 COVID-19 感染中细胞代谢介导的并发症。

SARS CoV-2 aggravates cellular metabolism mediated complications in COVID-19 infection.

机构信息

Mahatma Gandhi College of Pharmaceutical Sciences, Jaipur, India.

School of Pharmacy, Suresh Gyan Vihar University, Jaipur, India.

出版信息

Dermatol Ther. 2020 Nov;33(6):e13871. doi: 10.1111/dth.13871. Epub 2020 Jul 7.

DOI:10.1111/dth.13871
PMID:32558055
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7323108/
Abstract

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the primary causative organism in corona virus disease-19 (COVID-19) infections, is a novel member of the human coronavirus family which was first identified in Wuhan, China, towards the end of 2019. This letter reveals new vital missing links in our current understanding of the mechanisms that lead to cell death triggered by ferroptotic stress in COVID-19 infection. It further reveal the importance of homocysteine mediated trans-sulfuration pathway in COVID-19 infection. Hence, Vitamin B6, folic acid, and Vitamin B12 should be incorporated in the treatment regimen for SARS CoV-2 infections to suppress complications, as the virus mediates altered host cell metabolism.

摘要

严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）是导致 2019 年冠状病毒病（COVID-19）感染的主要病原体，是人类冠状病毒家族中的一种新型成员，于 2019 年底在中国武汉首次被发现。这封信揭示了我们目前对 COVID-19 感染导致细胞死亡的机制的理解中缺失的重要环节。它进一步揭示了同型半胱氨酸介导的转硫途径在 COVID-19 感染中的重要性。因此，维生素 B6、叶酸和维生素 B12 应该被纳入 SARS CoV-2 感染的治疗方案中，以抑制病毒介导的宿主细胞代谢改变所导致的并发症。

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Covid-19, Angiogenesis, and ARDS Endotypes.新型冠状病毒肺炎、血管生成与急性呼吸窘迫综合征的内型
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