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Purpose <p>Vascular calcification (VC) represents a pathological hallmark of diseases such as chronic kidney disease (CKD) and diabetes, driven by the dysregulated activity of matrix vesicles (MVs). Under physiological conditions, MVs orchestrate skeletal mineralization, but in pathological microenvironments characterized by hyperphosphatemia and inflammation, they initiate and propagate ectopic calcification within the vascular wall. This review systematically examines the dual role of MVs—as both drivers of pathology and potential therapeutic vectors.</p> Methods <p>We detail two strategic approaches: engineering MVs into targeted delivery systems for anti-calcific agents, and developing selective inhibitors against key molecular regulators of the MV lifecycle.</p> Results <p>By integrating mechanistic insights with translational perspectives, we propose an innovative “mechanism–biomarker–drug–delivery” framework that advances the development of precise, MV-based therapeutics.</p> Conclusion <p>This work not only clarifies the pivotal role of MVs in VC but also charts a promising pathway toward clinically viable interventions, highlighting MVs as central targets in the future of precision medicine for VC.</p>

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From Mechanism to Therapy: Establishing an Integrated Framework for the Regulation and Intervention of Matrix Vesicles in Vascular Calcification

  • 期刊论文

  • 发表日期：

    2026年4月27日

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  • Mincheng Yu,
  • Jingzheng Chen,
  • Xinyue Wang,
  • Ling Chen,
  • Xiaomei Ren,
  • Mayibai Mushajiang,
  • Liqun Ren,
  • Zhongqun Wang

摘要

Purpose

Vascular calcification (VC) represents a pathological hallmark of diseases such as chronic kidney disease (CKD) and diabetes, driven by the dysregulated activity of matrix vesicles (MVs). Under physiological conditions, MVs orchestrate skeletal mineralization, but in pathological microenvironments characterized by hyperphosphatemia and inflammation, they initiate and propagate ectopic calcification within the vascular wall. This review systematically examines the dual role of MVs—as both drivers of pathology and potential therapeutic vectors.

Methods

We detail two strategic approaches: engineering MVs into targeted delivery systems for anti-calcific agents, and developing selective inhibitors against key molecular regulators of the MV lifecycle.

Results

By integrating mechanistic insights with translational perspectives, we propose an innovative “mechanism–biomarker–drug–delivery” framework that advances the development of precise, MV-based therapeutics.

Conclusion

This work not only clarifies the pivotal role of MVs in VC but also charts a promising pathway toward clinically viable interventions, highlighting MVs as central targets in the future of precision medicine for VC.