From angiotensin-converting enzyme 2 disruption to thromboinflammatory microvascular disease: A paradigm drawn from COVID-19

Autor: Giulio Russo, Daniela Pedicino, Felicita Andreotti, Filippo Crea, Ramona Vinci, Alessia D’Aiello, Giovanna Liuzzo, R De Cristofaro
Jazyk: angličtina
Rok vydání: 2021
Předmět:
ACEI
ACE inhibitors

Disease
030204 cardiovascular system & hematology
von Willebrand factor
medicine.disease_cause
Renin-Angiotensin System
0302 clinical medicine
CCL
C-C-motif chemokine ligand

GCSF
granulocyte-colony stimulating factor

Medicine
030212 general & internal medicine
COVID-19
2019 coronavirus disease

C
complement component

Coronavirus
TNF
tumor necrosis factor

biology
2019 coronavirus
ICU
intensive care unit

PCT
procalcitonin

ARB
angiotensin receptor blocker

TMPRSS2
transmembrane serine protease type II

PAI-1
plasminogen activator inhibitor-1

Angiotensin-converting enzyme 2
CRP
C-reactive protein

MAC
membrane attack complex

Angiotensin-Converting Enzyme 2
Inflammation Mediators
Cardiology and Cardiovascular Medicine
MIP
macrophage inflammatory protein

VWF
von Willebrand factor

IP
interferon-gamma inducible protein

ACE
angiotensin-converting enzyme

CD
cluster of differentiation

SARS-CoV
severe acute respiratory syndrome coronavirus

Ischemia
Complement
Article
t-PA
tissue-type plasminogen activator

03 medical and health sciences
Von Willebrand factor
Humans
IFN
interferon

NO
nitric oxide

Thromboinflammatory microangiopathy
business.industry
Microangiopathy
COVID-19
RAS
renin-angiotensin system

Angiotensin-converting enzyme
Thrombosis
MCP
monocyte chemoattractant protein

medicine.disease
ANG
angiotensin

IL
interleukin

TF
tissue factor

Microvessels
Settore MED/11 - MALATTIE DELL'APPARATO CARDIOVASCOLARE
biology.protein
business
Complement membrane attack complex
Neuroscience
Zdroj: International Journal of Cardiology
Popis: We concisely review clinical, autopsy, experimental and molecular data of 2019 coronavirus disease (COVID-19). Angiotensin-converting enzyme 2 disruption and thromboinflammatory microangiopathy emerge as distinctive features. Briefly, entry of the virus into microvessels can profoundly disrupt the local renin-angiotensin system, cause endothelial injury, activate the complement cascade and induce powerful thromboinflammatory reactions, involving, in particular, von Willebrand factor, that, if widespread, may lead to microvascular plugging, ischemia and, ultimately, organ failure. We believe the current COVID-19 data consolidate a widely unrecognised paradigm of potentially fatal thromboinflammatory microvascular disease.
Highlights • SARS-CoV-2 entry into microvessels can disrupt the local renin-angiotensin-system. • Complement and von Willebrand factor overexpression occur in COVID-19. • COVID-19 patients show widespread thromboinflammatory microvascular disease. • COVID-19 provides an important paradigm of potentially fatal microangiopathy.
Databáze: OpenAIRE