Corpus overview


Overview

MeSH Disease

Transmission

gender (1)


Seroprevalence

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    Hypothesis: mPGES-1-Derived Prostaglandin E2, a So Far Missing Link in COVID-19 MESHD Pathophysiology?

    Authors: Jan Smeitink; Xiaolan Jiang; Svetlana Pecheritsyna; Herma Renkema; Rob van Maanen; Julien Beyrath

    id:10.20944/preprints202004.0180.v1 Date: 2020-04-12 Source: Preprints.org

    With frequencies varying up to 20%, treatment resistant pulmonary failure MESHD is a major life-threatening complication in COVID-19 MESHD (SARS-CoV-2, HCoV19) disease pathology. Both acute respiratory distress syndrome MESHD respiratory distress HP syndrome ( ARDS MESHD), proposed to be caused by an over-reacting immune system which floods the lung with edema HP edema MESHD, a liquid consisting of inflammatory cells, and diminished lung perfusion, have been postulated to cause this treatment resistant lung failure MESHD. Aging, co-morbidities, male TRANS gender TRANS and obesity HP obesity MESHD are pre-existing factors associated with the more severe outcome. Thrombosis MESHD is more frequently observed than usually seen during ICU admission. Different hypotheses explaining the pathophysiological cascade leading to fast progressing severe COVID-19 MESHD disease and how to counteract it have been proposed. A variety of intervention studies to control severity are ongoing or planned. Not suggested so far, we here hypothesize that the inflammatory lipid modulator prostaglandin E2 (PGE2) executes a prominent role in COVID-19 MESHD pathophysiology. Based on this we suggest measuring PGE2 in patients and evaluating selective inhibition of the human microsomal prostaglandin E synthase-1 (mPGES-1) as a potential innovative therapeutic approach in this devastating condition for which sonlicromanol, a drug currently in phase 2b studies for mitochondrial disease MESHD, is a candidate.

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MeSH Disease
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