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Arterial Stiffness and the Canonical WNT/β-catenin Pathway

  • Mechanisms of Hypertension and Target-Organ Damage (JE Hall and ME Hall, Section Editors)
  • Published:
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Abstract

Purpose of Review

Arterial stiffness (AS) was mainly associated with cardiovascular morbidity and mortality in a hypertensive patient. Some risk factors contribute to the development of AS, such as aging, high blood pressure, vascular calcification, inflammation, and diabetes mellitus. The WNT/β-catenin pathway is implicated in numerous signaling and regulating pathways, including embryogenesis, cell proliferation, migration and polarity, apoptosis, and organogenesis. The activation of the WNT/β-catenin pathway is associated with the development of these risk factors.

Recent Findings

Aortic pulse wave velocity (PWV) is measured to determine AS, and in peripheral artery disease patients, PWV is higher than controls. An augmentation in PWV by 1 m/s has been shown to increase the risk of cardiovascular events by 14%. AS measured by PWV is characterized by the deregulation of the WNT/β-catenin pathway by the inactivation of its two inhibitors, i.e., DKK1 and sclerostin.

Summary

Thus, this review focuses on the role of the WNT/β-catenin pathway which contributes to the development of arterial stiffness.

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Abbreviations

Acetyl-coA:

Acetyl-coenzyme A

APC:

Adenomatous polyposis coli

ECM:

Extracellular matrix

FZD:

Frizzled

GSK-3β:

Glycogen synthase kinase-3β

LRP 5/6:

Low-density lipoprotein receptor-related protein 5/6

NF-ϰB:

Nuclear factor kappaB

TCF/LEF:

T-cell factor/lymphoid enhancer factor

TNF-α:

Tumor necrosis factor alpha

VSMC:

Vascular smooth muscle cell

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Vallée, A. Arterial Stiffness and the Canonical WNT/β-catenin Pathway. Curr Hypertens Rep 24, 499–507 (2022). https://doi.org/10.1007/s11906-022-01211-7

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