# Augmented Flow-Induced Outward Remodelling Occurs with Ageing in Mice

**Authors:** Bethan Brown, Helen Williams, Samson Egbulonu, Andrew Bond, Jason Johnson, Sarah George

PMC · DOI: 10.3390/ijms262110274 · 2025-10-22

## TL;DR

This study shows that aging in mice leads to more pronounced outward artery remodeling, which could contribute to cardiovascular diseases like atherosclerosis and aneurysms.

## Contribution

The study reveals that aging enhances positive arterial remodeling in mice, potentially increasing disease risk.

## Key findings

- Older mice showed greater lumen expansion and reduced medial thickness after artery ligation.
- Arteries from old mice had decreased α-SM-actin content per cell and collagen.
- MMP-2 protein increase was observed only in young mice during remodeling.

## Abstract

Outward remodelling of arteries is a feature of cardiovascular pathologies such as atherosclerosis and aneurysm, so a greater understanding of the processes involved in remodelling may aid the development of improved therapies for patients. As ageing increases the risk of atherosclerosis and aneurysmal disease, it was therefore hypothesised that ageing affects arterial remodelling and thereby contributes to these diseases. To test this hypothesis, we compared right carotid artery remodelling in young (2 months, n = 13) and old (18–20 months, n = 13) mice resulting from increased blood flow after ligation of the left carotid artery. The media area, thickness, collagen content and α-SM-actin content per cell of control right carotid arteries from old mice were significantly greater than observed in young mice. Positive remodelling was observed in the carotid arteries of both old and young mice 21 days after ligation of the left carotid artery. However, arteries from old mice had a significantly larger increase in lumen size and reduction in media area, thickness and α-SM-actin content per cell compared to young arteries, indicative of augmented positive remodelling in arteries from old mice. Remodelling was associated with significantly increased MMP-2 protein in arteries from young mice, but this was not observed in arteries from old mice. This study demonstrates that the extent of positive remodelling of carotid arteries is greater in old mice than in young mice and results in a potentially less resilient medial layer with decreased α-SM-actin content per cell, elastin and collagen that may promote atherosclerosis and aneurysm formation.

## Linked entities

- **Proteins:** MMP2 (matrix metallopeptidase 2)
- **Diseases:** atherosclerosis (MONDO:0005311)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Eln (elastin) [NCBI Gene 13717] {aka E030024M20Rik}, Mmp2 (matrix metallopeptidase 2) [NCBI Gene 17390] {aka Clg4a, GelA, MMP-2}
- **Diseases:** Outward Remodelling (MESH:D020257), arterial remodelling (MESH:D066253), arteries (MESH:D012078), cardiovascular pathologies (MESH:D002318), aneurysm (MESH:D000783), atherosclerosis (MESH:D050197)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12610229/full.md

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Source: https://tomesphere.com/paper/PMC12610229