Related Experiment Video
Updated: Jan 2, 2026

Analyzing Platelet Subpopulations by Multi-color Flow Cytometry
Published on: June 10, 2025
Platelet Function in Cardiovascular Disease: Activation of Molecules and Activation by Molecules
1Health Research Institute, Research Center of Thalassemia & Hemoglobinopathy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. elahehkhodadi@gmail.com.
Insights
Platelets are crucial in cardiovascular disease (CVD) development. Targeting molecules involved in platelet activation offers potential therapeutic strategies for reducing thrombosis and atherosclerosis in CVD patients.
Area of Science:
- Cardiovascular Biology
- Hematology
- Molecular Medicine
Background:
- Cardiovascular disease (CVD) is a leading global cause of mortality.
- Platelets play a critical role in the pathogenesis of thrombosis and atherosclerosis, key contributors to CVD.
- Platelet activation is a complex process influenced by various factors including lipids, inflammatory mediators, peptide hormones, microRNAs (miRNAs), and oxidative stress.
Purpose of the Study:
- To review the molecules involved in platelet activation in the context of CVD.
- To identify molecules activated by platelets that contribute to CVD.
- To discuss the potential of targeting these molecules for therapeutic interventions against thrombosis and atherosclerosis.
Main Methods:
- Literature review focusing on molecular mechanisms of platelet activation in CVD.
- Analysis of studies investigating platelet-surface molecule interactions and their role in inflammation and thrombosis.
- Synthesis of information on potential therapeutic targets for CVD management.
Main Results:
- Platelet activation is modulated by diverse molecular entities, including lipids, signaling proteins, miRNAs, and oxidative stress.
- Surface molecules on activated platelets mediate interactions with other cells and chemokines, promoting inflammation and thrombosis.
- Specific molecules involved in platelet activation or activated by platelets show promise as predictive markers for CVD outcomes.
Conclusions:
- Identifying and targeting molecules that regulate platelet activation and interaction is a promising strategy for managing CVD.
- Dual therapy, combining receptor blockers with novel drugs, may enhance the clinical management of CVD patients.
- Further research into these molecular players can lead to novel therapeutic approaches to reduce thrombosis and atherosclerosis.
Abstract:
Globally, one of the major causes of death is the cardiovascular disease (CVD), and platelets play an important role in thrombosis and atherosclerosis that led to death. Platelet activation can be done by different molecules, genes, pathways, and chemokines. Lipids activate platelets by inflammatory factors, and platelets are activated by receptors of peptide hormones, signaling and secreted proteins, microRNAs (miRNAs), and oxidative stress which also affect the platelet activation in older age. In addition, surface molecules on platelets can interact with other cells and chemokines in activated platelets and cause inflammation thrombosis events and CVD. However, these molecules activating platelets or being activated by platelets can be suggested as the markers to predict the clinical outcome of CVD and can be targeted to reduce thrombosis and atherosclerosis. However, hindering these molecules by other factors such as genes and receptors can reduce platelet activation and aggregation and targeting these molecules can control platelet interactions, thrombosis, and CVD. In addition, dual therapy with the receptor blockers and novel drugs results in better management of CVD patients. Overall, our review will emphasize on the molecules involved in the activation of platelets and on the molecules that are activated by platelets in CVD and discuss the molecules that can be blocked or targeted to reduce the thrombosis events and control CVD.
Related Concept Videos
Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Structure and Function of Platelets
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000...
Anticoagulant Drugs: Low-Molecular-Weight Heparins
Extrinsic and Intrinsic Pathways of Hemostasis
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
Clot Retraction and Fibrinolysis
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...

