Little is known about the mechanism of coronavirus disease 2019 (COVID-19)-induced critical illness and death. The host infection mediated by SARS-CoV-2 is mainly relied on ACE2 receptor. There is still a lack of clinical data about the effects of interaction of ACE2 and SARS-CoV-2 on RAS system and disease progression. We investigated the plasma angiotensin II (Ang II) and renin levels in 82 non-hypertensive patients (42 mild cases, 25 severe cases, and 15 critically ill cases) infected by SARS-CoV-2 and 12 critically ill patients not infected by SARS-CoV-2 serving as control. Plasma Ang II level was higher than that of normal range in the majority of COVID-19 cases (90.2%), especially the plasma Ang II positive rate in the critically ill COVID-19 patients (100%). Plasma Ang II level in critically ill COVID-19 patients was significantly higher than that of control and those with mild COVID-19 symptoms (Fig. 1). Univariate analysis indicated a positive correlation between plasma Ang II level and COVID-19 severity. Partial SARS-CoV-2 patients (12.2%) showed elevation of renin content than normal range. There were no statistical differences in renin among the mild, severe, and appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material.
Our results suggest that BDNF DNA hypomethylation and its interaction with lower LES score might result in impaired antidepressant treatment response. The pharmacoepigenetic study could eventually help in finding epigenetic biomarkers of antidepressant response.
The mTOR signaling pathways regulate cell growth and are involved in multiple human diseases. Here, we identify UBTOR, a previously unannotated gene as a functional player in regulating cell growth and mTOR signaling. Reduction of UBTOR function in cultured hippocampal neurons and PC12 cells promotes neurite outgrowth. UBTOR depletion activates mTOR signaling and promotes cell growth, whilst UBTOR overexpression suppresses colony formation in cancer cell lines. Studies in cultured cells and zebrafish model show that UBTOR inhibits mTOR signaling by stabilizing the mTOR complex component DEPTOR, and ubtor gene disruption result in higher mTOR activity and aggravate HRAS(G12V) induced neoplasia in the zebrafish. Lastly, UBTOR depletion promotes tumor growth and mTOR signaling in a xenograft mouse model. Together, our results demonstrate how UBTOR regulates cell growth and neoplasia via mTOR signaling.
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