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Platelets in Vascular Calcification: A Comprehensive Review of Platelet-Derived Extracellular Vesicles, Protein
Yi He1, Qiongyue Zhang2, Lina Pan1
1Department of Cardiology, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Insights
Platelets directly contribute to vascular calcification, a condition linked to atherosclerosis and cardiovascular events. Targeting platelet mechanisms offers new therapeutic avenues for managing arterial stiffening and related complications.
Area of Science:
- Cardiovascular Biology
- Vascular Biology
- Platelet Biology
Background:
- Vascular calcification (VC) is a hallmark of atherosclerosis, increasing risks of stroke and myocardial infarction.
- Severe VC complicates interventional procedures, raising risks of adverse cardiovascular events.
- Platelets are known to promote atherosclerosis through inflammatory and cellular processes.
Purpose of the Study:
- To critically assess the emerging evidence for a direct role of platelets in vascular calcification.
- To elucidate the intricate mechanisms by which platelets contribute to VC.
- To identify potential therapeutic targets within platelet pathways for managing VC.
Main Methods:
- This review synthesizes current literature on platelet involvement in VC.
- Focuses on mechanisms including extracellular vesicles, platelet-regulatory proteins, and platelet function indices.
- Evaluates the potential for therapeutic targeting of these platelet-related pathways.
Main Results:
- Platelets actively promote vascular calcification through various secreted factors and cellular interactions.
- Extracellular vesicles released by platelets play a significant role in VC.
- Platelet-regulatory proteins and specific functional indices are implicated in the VC process.
Conclusions:
- Platelets are direct contributors to vascular calcification, not just passive bystanders in atherosclerosis.
- Understanding these mechanisms opens novel therapeutic strategies targeting platelet activity.
- Interventions aimed at platelet pathways may mitigate VC progression and associated cardiovascular risks.
Abstract:
Vascular calcification (VC) commonly accompanies the development of atherosclerosis, defined by the accumulation of calcium in the arterial wall, potentially leading to stroke and myocardial infarction. Severe and unevenly distributed calcification poses challenges for interventional procedures, elevating the risks of vascular dissection, acute vascular occlusion, restenosis, and other major adverse cardiovascular events. Platelets promote the development of atherosclerosis by secreting various inflammatory mediators, regulating cell migration, aggregation, adhesion, and initiating and expanding inflammatory responses. There is emerging evidence that platelets play a direct role in VC; however, this novel concept has not yet been critically assessed. This review describes the intricate mechanisms by which platelets promote VC, focusing on three key aspects and the potential opportunities for their therapeutic targeting: extracellular vesicles, platelet-regulatory proteins, and indices related to platelet function.
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