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Updated: Aug 16, 2025

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Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
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Interleukin-29 Accelerates Vascular Calcification via JAK2/STAT3/BMP2 Signaling
Nannan Hao1, Zihao Zhou1, Feifei Zhang1
1Department of Cardiology The First Affiliated Hospital of Nanjing Medical University Nanjing Jiangsu Province China.
Journal of the American Heart Association
|December 20, 2022
Summary
Interleukin-29 (IL-29) promotes vascular calcification by activating inflammatory pathways. Inhibiting IL-29 or its receptor may offer new treatments for vascular diseases.
Area of Science:
- Cardiovascular Biology
- Immunology
- Cell Biology
Background:
- Vascular calcification (VC) increases cardiovascular risk and involves smooth muscle cell osteogenic transdifferentiation.
- Inflammation is a key driver in the initiation and progression of VC.
- Interleukin-29 (IL-29), a type III interferon, is implicated in autoimmune diseases.
Purpose of the Study:
- To investigate the role of IL-29 in vascular calcification.
- To elucidate the underlying inflammatory mechanisms involving IL-29 in VC.
Main Methods:
- Measured IL-29 and BMP2 mRNA and protein levels in human calcified arteries.
- Assessed IL-29 effects on rat vascular smooth muscle cell proliferation, apoptosis, and migration in vitro.
- Evaluated IL-29's impact on rat aortic ring calcification ex vivo.
- Utilized pharmacological inhibition of IL-29/IL-28Rα and JAK2/STAT signaling pathways.
Main Results:
- IL-29 mRNA expression correlated positively with BMP2 in calcified human arteries.
- IL-29 promoted vascular smooth muscle cell osteogenic transdifferentiation and calcification in vitro and ex vivo.
- IL-29's procalcification effects were mediated via the JAK2/STAT3 pathway and reduced BMP2 expression.
- IL-29 inhibited vascular smooth muscle cell proliferation without affecting apoptosis or migration.
Conclusions:
- IL-29 plays a significant role in vascular calcification development.
- The JAK2/STAT3 signaling pathway is involved in IL-29-mediated VC.
- Targeting IL-29 or its receptor IL-28Rα presents a potential therapeutic strategy for VC.
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