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

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.