# The role of microRNAs in calcific aortic valve disease

**Authors:** Yi-Zhou Peng, Yang He, Yue-Jiao Yang, Liang Tang

PMC · DOI: 10.3389/fcvm.2025.1637753 · 2026-01-09

## TL;DR

This paper reviews how microRNAs influence calcific aortic valve disease, offering potential for new treatments and biomarkers.

## Contribution

The paper systematically reviews miRNA roles in CAVD pathophysiology and their potential as biomarkers or therapeutic targets.

## Key findings

- miRNAs regulate endothelial dysfunction, inflammation, and extracellular matrix remodeling in CAVD.
- Shared miRNA regulators exist between CAVD and osteoporosis, suggesting common mechanisms.
- miRNA-mediated pathways could lead to novel biomarkers and therapies for CAVD.

## Abstract

Calcific aortic valve disease (CAVD) is a prevalent and progressive valvular disorder characterized by fibrocalcific remodeling and eventual valve stenosis. Despite its clinical burden, current treatment is limited to valve replacement at end-stage disease, with no approved medical therapy to slow or halt its progression. Increasing evidence suggests that microRNAs (miRNAs), small non-coding RNAs that post-transcriptionally regulate gene expression, are critically involved in the pathophysiology of CAVD. This review highlights the roles of key miRNAs in CAVD, focusing on their involvement in endothelial dysfunction, inflammation, extracellular matrix remodeling, and the osteogenic differentiation of valvular interstitial cells. Furthermore, we explore the intersection between CAVD and osteoporosis, two diseases that share overlapping pathophysiological mechanisms and miRNA regulators. Understanding miRNA-mediated pathways in CAVD may uncover novel biomarkers and therapeutic targets to delay disease progression and improve patient outcomes.

## Linked entities

- **Diseases:** osteoporosis (MONDO:0005298)

## Full-text entities

- **Diseases:** valve stenosis (MESH:D001024), osteoporosis (MESH:D010024), CAVD (OMIM:109730), valvular disorder (MESH:D000082862), endothelial dysfunction (MESH:D014652), inflammation (MESH:D007249)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12827586/full.md

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Source: https://tomesphere.com/paper/PMC12827586