ArticleArchives of medical science : AMS2021
Game of "crowning" season 8: RAS and reproductive hormones in COVID-19 - can we end this viral series?
Article in Archives of medical science : AMS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Promises and Pitfalls of Calcineurin Inhibitors in COVID-19: A Systematic Review and Meta-analysis of Controlled Trials.Current medicinal chemistry · 2024Pooled it
- COVID-19 in Poland: potential associations with epidemiology, population and healthcare quality.Archives of medical science : AMS · 2026Article
- COVID-19 disease: novel clinical manifestations and therapeutic exploration.Archives of medical science : AMS · 2026Article
- Molecular and pro-inflammatory aspects of COVID-19: The impact on cardiometabolic health.Biochimica et biophysica acta. Molecular basis of disease · 2022Review
- Molecular Docking and Dynamic Simulation Revealed the Potential Inhibitory Activity of Opioid Compounds Targeting the Main Protease of SARS-CoV-2.BioMed research international · 2022Article
- Hypertensive urgencies during the first wave of the COVID-19 pandemic in a tertiary hospital setting: a U-shaped alarming curve.Archives of medical science : AMS · 2022Article
- Multiple potential targets of opioids in the treatment of acute respiratory distress syndrome from COVID-19.Journal of cellular and molecular medicine · 2021Review
- Efficacy and harms of convalescent plasma for treatment of hospitalized COVID-19 patients: a systematic review and meta-analysis.Archives of medical science : AMS · 2021Article
- Measurement of oxidized albumin: An opportunity for diagnoses or treatment of COVID-19.Bioorganic chemistry · 2020Article
- Cholesterol in Relation to COVID-19: Should We Care about It?Journal of clinical medicine · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The outbreak of a newly identified coronavirus, the SARS-CoV-2 (alternative name 2019-nCoV), capable of jumping across species causing zoonosis with severe acute respiratory syndromes (SARS), has alerted authorities worldwide. Soon after the epidemic was first detected in the city of Wuhan in the Hubei Province of China, starting in late December 2019, the virus spread over multiple countries in different continents, being declared a pandemic by March 2020. The demographic characteristics of the infected patients suggest that age, sex, and comorbidities are predictive factors for the fatality of the infection. The mechanisms of viral entry into the human host cells seem to be in a close relationship with the mechanisms of regulating the renin-angiotensin system (RAS), which may explain the pathogenesis associated with the infection. This brings new insights into the possibilities of exploiting viral entry mechanisms to limit associated complications by means of enhancing the resistance of the infected patients using methods of regulating the RAS and strategies of modulating ACE2 expression. In this perspective article we exploit the mechanisms of COVID-19 pathogenesis based on the demographic characteristics of the infected patients reported in the recent literature and explore several approaches of limiting the initial steps of viral entry and pathogenesis based on viral interactions with ACE2 and RAS. We further discuss the implications of reproductive hormones in the regulation of the RAS and investigate the premise of using endocrine therapy against COVID-19.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.