Pulmonary Artery Thrombosis: A Diagnosis That Strives for Its Independence

Autor: Sergey Saiganov, Vladimir Tomson, Yana Toropova, Alexander Brill, Kirill Lobastov, Olga Yaroslavna Porembskaya, Leonid Laberko, Viacheslav Nikolaevich Kravchuk
Rok vydání: 2020
Předmět:
0301 basic medicine
pulmonary embolism
Receptor expression
Receptor for Advanced Glycation End Products
Review
030204 cardiovascular system & hematology
lcsh:Chemistry
0302 clinical medicine
Cell-Derived Microparticles
Risk Factors
Medicine
Platelet
Endothelial dysfunction
HMGB1 Protein
prothrombotic phenotype
lcsh:QH301-705.5
Spectroscopy
pulmonary artery thrombosis
General Medicine
Thrombosis
Cell Hypoxia
Computer Science Applications
medicine.anatomical_structure
Cardiology
Cytokines
medicine.symptom
Blood Platelets
medicine.medical_specialty
Endothelium
Nitric Oxide Synthase Type III
Pulmonary Artery
Catalysis
Inorganic Chemistry
03 medical and health sciences
medicine.artery
Internal medicine
Humans
Receptor
PAR-1
Platelet activation
Physical and Theoretical Chemistry
Molecular Biology
business.industry
Organic Chemistry
Hypoxia (medical)
medicine.disease
Platelet Activation
030104 developmental biology
lcsh:Biology (General)
lcsh:QD1-999
Pulmonary artery
Endothelium
Vascular
business
Zdroj: International Journal of Molecular Sciences
International Journal of Molecular Sciences, Vol 21, Iss 5086, p 5086 (2020)
ISSN: 1422-0067
Popis: According to a widespread theory, thrombotic masses are not formed in the pulmonary artery (PA) but result from migration of blood clots from the venous system. This concept has prevailed in clinical practice for more than a century. However, a new technologic era has brought forth more diagnostic possibilities, and it has been shown that thrombotic masses in the PA could, in many cases, be found without any obvious source of emboli. Chronic obstructive pulmonary disease, asthma, sickle cell anemia, emergency and elective surgery, viral pneumonia, and other conditions could be complicated by PA thrombosis development without concomitant deep vein thrombosis (DVT). Different pathologies have different causes for local PA thrombotic process. As evidenced by experimental results and clinical observations, endothelial and platelet activation are the crucial mechanisms of this process. Endothelial dysfunction can impair antithrombotic function of the arterial wall through downregulation of endothelial nitric oxide synthase (eNOS) or via stimulation of adhesion receptor expression. Hypoxia, proinflammatory cytokines, or genetic mutations may underlie the procoagulant phenotype of the PA endothelium. Both endotheliocytes and platelets could be activated by protease mediated receptor (PAR)- and receptors for advanced glycation end (RAGE)-dependent mechanisms. Hypoxia, in particular induced by high altitudes, could play a role in thrombotic complications as a trigger of platelet activity. In this review, we discuss potential mechanisms of PA thrombosis in situ.
Databáze: OpenAIRE
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