Endothelial Phenotype Transition and Vascular Calcification Mechanisms
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: 31 July 2026 | Viewed by 28
Special Issue Editors
2. Department of Physiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
3. Department of Orthopedic Surgery, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
Interests: vascular calcification; atherosclerosis; inflammation; osteoporosis
2. Department of Bioengineering, University of California, Los Angeles, CA, USA
3. Department of Medicine, Greater Los Angeles VA Healthcare System, Los Angeles, CA 90073, USA
Interests: endothelial-to-mesenchymal transition; cardiovascular calcification; heart failure; sports cardiology
Special Issue Information
Dear Colleagues,
Vascular calcification is a tightly regulated, cell-mediated process that contributes to cardiovascular morbidity and mortality across a wide spectrum of diseases. Once considered a passive degenerative phenomenon, both intimal calcification associated with atherosclerosis and medial calcification characteristic of aging, diabetes, and chronic kidney disease are now recognized as active processes driven by the phenotypic plasticity of vascular cells. Among these, endothelial-to-mesenchymal transition (EndMT) has emerged as a critical mechanism linking vascular injury, inflammation, and disturbed metabolic homeostasis to calcific remodeling.
During EndMT, endothelial cells lose characteristic markers and functions while acquiring mesenchymal and osteogenic features, enabling their contribution to extracellular matrix remodeling, inflammatory signaling, and mineral deposition. Dysregulated signaling pathways—including TGF-β, BMP, Wnt, oxidative stress-responsive networks, and mechanotransduction pathways—promote EndMT and intersect with processes governing osteogenic differentiation and calcification morphology. Importantly, EndMT-derived cells may differentially influence micro- versus macro-calcification, with implications for plaque vulnerability and vascular stiffness.
This Special Issue, entitled “Endothelial Phenotype Transition and Vascular Calcification Mechanisms,” invites original research and review articles that elucidate the molecular, metabolic, and biomechanical drivers of EndMT in vascular calcification and explore emerging therapeutic strategies targeting endothelial plasticity to mitigate cardiovascular disease.
Dr. Yin Tintut
Dr. Jeffrey J. Hsu
Guest Editors
Manuscript Submission Information
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Keywords
- endothelial cell
- vascular calcification
- cell plasticity
- endothelial-to-mesenchymal transition (EndMT)
- vascular biology
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