Targeting thromboinflammation in COVID-19 - A narrative review of the potential of C1 inhibitor to prevent disease progression.
Antibodies, Monoclonal
Anticoagulants
/ therapeutic use
Antiviral Agents
/ therapeutic use
Complement C1 Inhibitor Protein
/ therapeutic use
Disease Progression
Endothelial Cells
Humans
Inflammation
/ drug therapy
Kallikreins
Kinins
SARS-CoV-2
Thromboinflammation
Thrombosis
/ drug therapy
COVID-19 Drug Treatment
C1 inhibitor
COVID-19
Complement system
Contact activation system
Kallikrein-kinin system
Thromboinflammation
Journal
Molecular immunology
ISSN: 1872-9142
Titre abrégé: Mol Immunol
Pays: England
ID NLM: 7905289
Informations de publication
Date de publication:
10 2022
10 2022
Historique:
received:
09
05
2022
revised:
07
08
2022
accepted:
15
08
2022
pubmed:
29
8
2022
medline:
21
9
2022
entrez:
28
8
2022
Statut:
ppublish
Résumé
Coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 is associated with a clinical spectrum ranging from asymptomatic carriers to critically ill patients with complications including thromboembolic events, myocardial injury, multisystemic inflammatory syndromes and death. Since the beginning of the pandemic several therapeutic options emerged, with a multitude of randomized trials, changing the medical landscape of COVID-19. The effect of various monoclonal antibodies, antiviral, anti-inflammatory and anticoagulation drugs have been studied, and to some extent, implemented into clinical practice. In addition, a multitude of trials improved the understanding of the disease and emerging evidence points towards a significant role of the complement system, kallikrein-kinin, and contact activation system as drivers of disease in severe COVID-19. Despite their involvement in COVID-19, treatments targeting these plasmatic cascades have neither been systematically studied nor introduced into clinical practice, and randomized studies with regards to these treatments are scarce. Given the multiple-action, multiple-target nature of C1 inhibitor (C1-INH), the natural inhibitor of these cascades, this drug may be an interesting candidate to prevent disease progression and combat thromboinflammation in COVID-19. This narrative review will discuss the current evidence with regards to the involvement of these plasmatic cascades as well as endothelial cells in COVID-19. Furthermore, we summarize the evidence of C1-INH in COVID-19 and potential benefits and pitfalls of C1-INH treatment in COVID-19.
Identifiants
pubmed: 36030710
pii: S0161-5890(22)00408-4
doi: 10.1016/j.molimm.2022.08.008
pmc: PMC9393183
pii:
doi:
Substances chimiques
Antibodies, Monoclonal
0
Anticoagulants
0
Antiviral Agents
0
Complement C1 Inhibitor Protein
0
Kinins
0
Kallikreins
EC 3.4.21.-
Types de publication
Journal Article
Review
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
99-113Informations de copyright
Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.
Déclaration de conflit d'intérêts
Conflict of interest Dr. Trendelenburg reports receiving grants from the Swiss National Science Foundation, Roche, Novartis, and Idorsia outside of the submitted work. Dr. Osthoff reports receiving grants from the Swiss National Science Foundation and Pharming Technologies B.V. for the investigator-initiated trial of rhC1INH in COVID-19 (ClinicalTrials.gov Identifier: NCT04414631), and from the Botnar Research Centre for Child Health outside the submitted work, and consulting fees from Pharming Technologies B.V. No other disclosures or conflicting interests with regards to this work have been reported.
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