# Modulation of CCR2/CCL2 molecular axis in the expansion and rupture of abdominal aortic aneurysms

## TL;DR

This paper reviews how targeting the CCR2/CCL2 pathway could help prevent and treat abdominal aortic aneurysms by reducing inflammation and aneurysm expansion.

## Contribution

The paper highlights the emerging role of CCR2 as a biomarker and therapeutic target for managing abdominal aortic aneurysms.

## Key findings

- CCR2 inhibition reduces AAA formation and progression in animal models.
- CCR2 is validated as a biomarker for AAA instability in humans using imaging techniques.
- Blocking CCR2 shows promise as a therapeutic strategy to prevent AAA rupture.

## Abstract

The CCR2/CCL2 molecular axis is a critical mediator of abdominal aortic aneurysm (AAA) pathogenesis. It has been demonstrated to drive chronic inflammation, extracellular matrix degradation, and vascular remodeling through the recruitment and activation of monocytes/macrophages and other immune cell types. Pre-clinical studies demonstrate that CCR2 inhibition reduces AAA formation, expansion, and progression in animal models. Emerging imaging techniques have validated CCR2 as a biomarker for AAA instability in humans. Although clinical trials targeting CCR2 are currently limited in number, ongoing translational studies highlight that CCR2 blockade is a promising therapeutic strategy to mitigate AAA expansion and the risk of rupture. This review underscores the potential of CCR2-targeting interventions to fill a critical unmet need to develop effective medical therapies for longitudinal clinical AAA management.