Related Experiment Video
Updated: May 15, 2025
In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time
Published on: May 24, 2020
Advanced Research in the Pathophysiology of Venous Thromboembolism-Acute Pulmonary Embolism
Anna M Imiela1, Joanna Kucharska1, Franciszek Kukliński2
1Department of Internal Diseases and Cardiology, Infant Jesus Clinical Hospital, Medical University of Warsaw, Lindleya 4 Street, 02-005 Warsaw, Poland.
Insights
Inflammation is a key risk factor for arterial and pulmonary embolism (APE). This review explores the roles of the endothelium, immune cells, and microRNAs in APE pathophysiology and potential therapeutic targets.
Area of Science:
- Cardiovascular Science
- Immunology
- Hematology
Background:
- Cardiovascular diseases (CVDs), including venous thromboembolism (VTE), are leading causes of global mortality.
- VTE pathophysiology is multifactorial, involving complex interactions similar to the Mosaic Theory of Hypertension.
- The concept of immunothrombosis highlights the interplay between the immune system and thrombosis.
Purpose of the Study:
- To review the role of inflammation as a risk factor for arterial and pulmonary embolism (APE).
- To elucidate the pathophysiology of APE, focusing on the endothelium, immune cells, and microRNAs (miRNAs).
- To explore potential therapeutic targets for APE.
Main Methods:
- Literature review of cardiovascular diseases, VTE, and immunothrombosis.
- Analysis of the interplay between immunity, coagulation, platelets, endothelium, reactive oxygen species (ROS), and genetic factors in APE.
- Examination of the specific roles of endothelial cells, immune cells, and miRNAs in APE pathogenesis.
Main Results:
- Inflammation is identified as a critical risk factor for APE.
- Immune mediators like monocytes and neutrophil extracellular traps (NETs) are crucial in thrombus formation.
- The endothelium, immune cells, and miRNAs are central to APE pathophysiology.
Conclusions:
- Immunity plays a central role in the complex pathophysiology of APE.
- Understanding the roles of the endothelium, immune cells, and miRNAs may reveal novel therapeutic strategies for APE.
- Further research into these pathways could lead to improved prevention and treatment of APE.
Abstract:
According to the literature, cardiovascular diseases (CVDs)-including myocardial infarction, stroke, and venous thromboembolism (VTE)-are among the leading causes of mortality and morbidity worldwide. Evidence suggests that CVDs share common risk factors and pathophysiological mechanisms. Similar to the Mosaic Theory of Hypertension proposed by Irvine Page in 1949, the pathophysiology of VTE is multifactorial, involving multiple interacting processes. The concept of immunothrombosis, introduced by Engelmann and Massberg in 2009, describes the interplay between the immune system and thrombosis. Both thrombosis and hemostasis share core mechanisms, including platelet activation and fibrin formation. Additionally, immune mediators-such as monocytes, neutrophil extracellular traps (NETs), lymphocytes, selectins, and various molecular factors-play a critical role in thrombus formation. This review highlights inflammation as a key risk factor for pulmonary embolism (APE). Immunity is central to the complex interactions among the coagulation cascade, platelets, endothelium, reactive oxygen species (ROS), and genetic factors. Specifically, we examine the roles of the endothelium, immune cells, and microRNAs (miRNAs) in the pathophysiology of APE and explore potential therapeutic targets. This review aims to elucidate the roles of the endothelium, immune cells, and miRNAs in the pathophysiology of APE and explore potential future perspective.
Related Concept Videos
01:30Anticoagulant Drugs: Low-Molecular-Weight Heparins
01:04Venous Return
What is Venous Return?
Venous return refers to the rate at which blood flows back to the heart from the body's peripheral veins. It's an integral part of the circulatory system...