Abstract

Large artery stiffness (LAS) is a major, independent risk factor underlying cardiovascular disease that increases with aging. The emergence of microRNA signaling as a key regulator of vascular structure and function has stimulated interest in assessing its role in the pathophysiology of LAS. Identification of several microRNAs that display age-associated changes in expression in aorta has focused attention on defining their molecular targets and deciphering their role in age-associated arterial stiffening. Inactivation of the microRNA-degrading enzyme, translin/trax, which reverses the age-dependent decline in miR-181b, confers protection from aging-associated arterial stiffening, suggesting that inhibitors targeting this enzyme may have translational potential. As LAS poses a major public health challenge, we anticipate that future studies based on these advances will yield innovative strategies to combat aging-associated arterial stiffening.

Highlights

  • The emergence of Large-Artery Stiffness (LAS) as a major risk factor for cardiovascular morbidity has stimulated interest in developing strategies to combat this endemic public health challenge (O’Rourke, 1990; Mitchell et al, 2010; Boutouyrie et al, 2011; O’Rourke et al, 2016; Chirinos et al, 2019)

  • The studies summarized above provide compelling evidence that alterations in microRNA signaling in aorta play a key role in the development of LAS

  • We have focused on their role in vascular smooth muscle cells (VSMCs)

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Summary

Introduction

The emergence of Large-Artery Stiffness (LAS) as a major risk factor for cardiovascular morbidity has stimulated interest in developing strategies to combat this endemic public health challenge (O’Rourke, 1990; Mitchell et al, 2010; Boutouyrie et al, 2011; O’Rourke et al, 2016; Chirinos et al, 2019).

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