Elevated Plasmin(ogen) as a Common Risk Factor for COVID-19 Susceptibility.
Identifieur interne : 000694 ( 2020/Analysis ); précédent : 000693; suivant : 000695Elevated Plasmin(ogen) as a Common Risk Factor for COVID-19 Susceptibility.
Auteurs : Hong-Long Ji [États-Unis] ; Runzhen Zhao [États-Unis] ; Sadis Matalon [États-Unis] ; Michael A. Matthay [États-Unis]Source :
- Physiological reviews [ 1522-1210 ] ; 2020.
Descripteurs français
- KwdFr :
- Comorbidité, Facteurs de risque, Fibrinolysine (métabolisme), Humains, Infections à coronavirus (mortalité), Infections à coronavirus (physiopathologie), Infections à coronavirus (sang), Infections à coronavirus (épidémiologie), Interactions hôte-pathogène (physiologie), Pandémies, Plasminogène (métabolisme), Pneumopathie virale (mortalité), Pneumopathie virale (physiopathologie), Pneumopathie virale (sang), Pneumopathie virale (épidémiologie), Susceptibilité à une maladie (sang), Syndrome de détresse respiratoire de l'adulte (physiopathologie), Syndrome de détresse respiratoire de l'adulte (sang), Syndrome de détresse respiratoire de l'adulte (virologie).
- MESH :
- mortalité : Infections à coronavirus, Pneumopathie virale.
- métabolisme : Fibrinolysine, Plasminogène.
- physiologie : Interactions hôte-pathogène.
- physiopathologie : Infections à coronavirus, Pneumopathie virale, Syndrome de détresse respiratoire de l'adulte.
- sang : Infections à coronavirus, Pneumopathie virale, Susceptibilité à une maladie, Syndrome de détresse respiratoire de l'adulte.
- virologie : Syndrome de détresse respiratoire de l'adulte.
- épidémiologie : Infections à coronavirus, Pneumopathie virale.
- Comorbidité, Facteurs de risque, Humains, Pandémies.
English descriptors
- KwdEn :
- Betacoronavirus (metabolism), Betacoronavirus (pathogenicity), Comorbidity, Coronavirus Infections (blood), Coronavirus Infections (epidemiology), Coronavirus Infections (mortality), Coronavirus Infections (physiopathology), Disease Susceptibility (blood), Fibrinolysin (metabolism), Host-Pathogen Interactions (physiology), Humans, Pandemics, Plasminogen (metabolism), Pneumonia, Viral (blood), Pneumonia, Viral (epidemiology), Pneumonia, Viral (mortality), Pneumonia, Viral (physiopathology), Respiratory Distress Syndrome, Adult (blood), Respiratory Distress Syndrome, Adult (physiopathology), Respiratory Distress Syndrome, Adult (virology), Risk Factors.
- MESH :
- chemical , metabolism : Fibrinolysin, Plasminogen.
- blood : Coronavirus Infections, Disease Susceptibility, Pneumonia, Viral, Respiratory Distress Syndrome, Adult.
- epidemiology : Coronavirus Infections, Pneumonia, Viral.
- metabolism : Betacoronavirus.
- mortality : Coronavirus Infections, Pneumonia, Viral.
- pathogenicity : Betacoronavirus.
- physiology : Host-Pathogen Interactions.
- physiopathology : Coronavirus Infections, Pneumonia, Viral, Respiratory Distress Syndrome, Adult.
- virology : Respiratory Distress Syndrome, Adult.
- Comorbidity, Humans, Pandemics, Risk Factors.
Abstract
Patients with hypertension, diabetes, coronary heart disease, cerebrovascular illness, chronic obstructive pulmonary disease, and kidney dysfunction have worse clinical outcomes when infected with SARS-CoV-2, for unknown reasons. The purpose of this review is to summarize the evidence for the existence of elevated plasmin(ogen) in COVID-19 patients with these comorbid conditions. Plasmin, and other proteases, may cleave a newly inserted furin site in the S protein of SARS-CoV-2, extracellularly, which increases its infectivity and virulence. Hyperfibrinolysis associated with plasmin leads to elevated D-dimer in severe patients. The plasmin(ogen) system may prove a promising therapeutic target for combating COVID-19.
DOI: 10.1152/physrev.00013.2020
PubMed: 32216698
Affiliations:
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pubmed:32216698Le document en format XML
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<term>Comorbidity</term>
<term>Coronavirus Infections (blood)</term>
<term>Coronavirus Infections (epidemiology)</term>
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<front><div type="abstract" xml:lang="en">Patients with hypertension, diabetes, coronary heart disease, cerebrovascular illness, chronic obstructive pulmonary disease, and kidney dysfunction have worse clinical outcomes when infected with SARS-CoV-2, for unknown reasons. The purpose of this review is to summarize the evidence for the existence of elevated plasmin(ogen) in COVID-19 patients with these comorbid conditions. Plasmin, and other proteases, may cleave a newly inserted furin site in the S protein of SARS-CoV-2, extracellularly, which increases its infectivity and virulence. Hyperfibrinolysis associated with plasmin leads to elevated D-dimer in severe patients. The plasmin(ogen) system may prove a promising therapeutic target for combating COVID-19.</div>
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