Platelet Function in Cardiovascular Disease: Activation of Molecules and Activation by Molecules

Elahe Khodadi1

  • 1Health Research Institute, Research Center of Thalassemia & Hemoglobinopathy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. elahehkhodadi@gmail.com.

Cardiovascular Toxicology
|December 1, 2019
PubMed

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.

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