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Impact of Perivascular Adipose Tissue on Neointimal Formation Following Endovascular Placement

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Abstract

Following the placement of endovascular implants, perivascular adipose tissue (PVAT) becomes an early sensor of vascular injury to which it responds by undergoing phenotypic changes characterized by reduction in the secretion of adipocyte-derived relaxing factors and a shift to a proinflammatory and pro-contractile state. Thus, activated PVAT loses its anti-inflammatory function, secretes proinflammatory cytokines and chemokines, and generates reactive oxygen species, which are accompanied by differentiation of fibroblasts into myofibroblasts and proliferation of smooth muscle cells. These subsequently migrate into the intima, leading to intimal growth. In addition, periadventitial vasa vasorum undergoes neovascularization and functions as a portal for extravasation of inflammatory infiltrates and mobilization of PVAT resident stem/progenitor cells into the intima. This review focuses on the response of PVAT to endovascular intervention-induced injury and discusses potential therapeutic targets to suppress the PVAT-initiated pathways that mediate the formation of neointima.

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Abbreviations

eNOS:

Endothelial nitric oxide synthase

Angptl2:

Angiopoietin-like protein 2

H2S:

Hydrogen sulfide

IL:

Interleukin

NADPH:

Nicotinamide adenine dinucleotide phosphate

NO:

Nitric oxide

MCP-1:

Monocyte chemoattractant protein-1

PVAT:

Perivascular tissue

PRDM16:

PR domain containing 16

ROS:

Reactive oxygen species

TNF-α:

Tumor necrosis factor-α

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Acknowledgements

We would like to thank Joanne Berger (FDA library) and Dr. Graeme O’May for editing the manuscript.

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Correspondence to Belay Tesfamariam.

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Tesfamariam, B. Impact of Perivascular Adipose Tissue on Neointimal Formation Following Endovascular Placement. J. of Cardiovasc. Trans. Res. (2024). https://doi.org/10.1007/s12265-024-10502-0

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