# Decoding vascular calcification: mechanistic insights and translational strategies

## TL;DR

This review explores the complex process of vascular calcification, its causes, and potential treatments, offering insights for future research and clinical applications.

## Contribution

The paper provides a comprehensive review of the mechanisms and therapeutic strategies for vascular calcification, emphasizing translational potential.

## Key findings

- Vascular calcification is linked to aging, atherosclerosis, chronic kidney disease, and diabetes.
- Recent advances in pharmacological and biomaterial-based interventions show promise for halting or reversing calcification.
- Extracellular vesicles, oxidative stress, and inflammation play key roles in vascular calcification mechanisms.

## Abstract

Vascular calcification (VC) is a complex, multifactorial process strongly associated with ageing, atherosclerosis, chronic kidney disease, and diabetes. Despite its clinical significance, effective treatment strategies remain elusive due to an incomplete understanding of the underlying mechanisms. In this review, we critically examine the cellular and molecular pathways that drive VC, including the transdifferentiation of vascular smooth muscle cells (VSMCs), the role of extracellular vesicles, and the influence of oxidative stress and inflammation. We also summarise key inducers and endogenous inhibitors of calcification, highlighting therapeutic targets currently under preclinical or clinical investigation. Notably, we evaluate recent advances in pharmacological and biomaterial-based interventions aimed at halting or reversing calcification, with a focus on their translational potential. By integrating mechanistic insights with therapeutic developments, this review offers a comprehensive perspective on VC pathophysiology and treatment, serving as a timely reference for future research and clinical innovation.

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