Platelets in Vascular Calcification: A Comprehensive Review of Platelet-Derived Extracellular Vesicles, Protein Interactions, Platelet Function Indices, and their Impact on Cellular Crosstalk

Author:

He Yi1,Zhang Qiongyue2,Pan Lina1,Yang Hao1,Liu Tao1,Bei Junjie3,Peter Karlheinz,Hu Houyuan1

Affiliation:

1. Department of Cardiology, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China

2. Department of Nephrology, Daping Hospital, Army Medical Center, Third Military Medical University (Army Medical University), Chongqing, China

3. Department of Cardiology, Guangxi Zhuang Autonomous Region Corps Hospital of People's Armed Police, Nanning, China

Abstract

AbstractVascular 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.

Publisher

Georg Thieme Verlag KG

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