Asset Details
Do you wish to reserve the book?
Advanced Research in the Pathophysiology of Venous Thromboembolism–Acute Pulmonary Embolism
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Advanced Research in the Pathophysiology of Venous Thromboembolism–Acute Pulmonary Embolism
Do you wish to request the book?
Advanced Research in the Pathophysiology of Venous Thromboembolism–Acute Pulmonary Embolism
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Advanced Research in the Pathophysiology of Venous Thromboembolism–Acute Pulmonary Embolism
2025
Overview
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.
