REVIEW article
Front. Cardiovasc. Med.
Sec. Atherosclerosis and Vascular Medicine
Volume 12 - 2025 | doi: 10.3389/fcvm.2025.1619018
This article is part of the Research TopicCardiovascular calcification: disease mechanisms, clinical phenotypes and therapeutic strategiesView all 5 articles
Interleukin Family in Vascular Calcification: Molecular Mechanisms and Therapeutic Perspectives
Provisionally accepted
- Vascular surgery department, Fuwai Yunnan Cardiovascular Hospital, Kunming City, China
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Vascular calcification (VC), characterized by pathological calcium deposition in arterial walls, is a major contributor to cardiovascular morbidity in chronic inflammatory diseases such as atherosclerosis, chronic kidney disease (CKD), and diabetes. Emerging evidence underscores the pivotal role of interleukin (IL) family cytokines in modulating VC through dual pro-and anti-calcific mechanisms. Proinflammatory IL members, including IL-1β, IL-6, IL-17A, and IL-29, drive osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs) by activating pathways such as NF-κB, STAT3, NLRP3 inflammasomes, and Wnt/βcatenin. These pathways upregulate osteogenic markers (e.g., Runx2, BMP-2) and promote oxidative stress, matrix remodeling, and pyroptosis. Conversely, antiinflammatory cytokines like IL-10 counteract calcification by suppressing inflammatory signaling, enhancing autophagy, and restoring mineral homeostasis. This review highlights the dynamic interplay between IL cytokines, metabolic dysregulation, and epigenetic modifications in VC pathogenesis. It advocates for multi-target approaches, such as combining TYK2/STAT3 inhibition with metabolic reprogramming, to disrupt pathological crosstalk. Future research must address spatiotemporal heterogeneity in IL signaling and optimize therapeutic specificity to translate mechanistic insights into clinical applications. Harnessing the IL family's dual roles offers transformative potential for mitigating VC while preserving immune integrity.
Keywords: interleukin family, Vascular Calcification, Osteogenic differentiation, Inflammation, therapeutic targets
Received: 27 Apr 2025; Accepted: 08 Jul 2025.
Copyright: © 2025 Zhao, Li and Guo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Yuanyuan Guo, Vascular surgery department, Fuwai Yunnan Cardiovascular Hospital, Kunming City, China
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