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Updated: Aug 5, 2025

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
Helicobacter Pylori Virulence Factor Cytotoxin-Associated Gene A (CagA) Induces Vascular Calcification in Coronary
Martin O Sundqvist1,2, Jonatan Wärme1,2, Robin Hofmann1,2
1Department of Clinical Science and Education, Division of Cardiology, Karolinska Institutet, Södersjukhuset, SE-118 83 Stockholm, Sweden.
Insights
Helicobacter pylori (H. pylori) infection may contribute to vascular calcification. The H. pylori CagA protein promotes osteogenic changes and calcification in coronary artery smooth muscle cells, indicating a potential cardiovascular risk.
Area of Science:
- Cardiovascular Biology
- Microbiology
- Cellular Biology
Background:
- Helicobacter pylori (H. pylori) infection is linked to cardiovascular diseases.
- The H. pylori virulence factor CagA is found in serum exosomes and may have systemic cardiovascular effects.
- The specific role of H. pylori and CagA in vascular calcification remains unclear.
Purpose of the Study:
- To investigate the vascular effects of CagA in human coronary artery smooth muscle cells (CASMCs).
- To assess CagA's impact on CASMC osteogenic gene expression, cellular calcification, and inflammatory responses.
Main Methods:
- Cultured human coronary artery smooth muscle cells (CASMCs).
- Exposed CASMCs to CagA.
- Measured osteogenic gene expression (e.g., BMP-2), interleukin-1β secretion, and cellular calcification.
Main Results:
- CagA upregulated bone morphogenic protein 2 (BMP-2) expression.
- CagA induced an osteogenic phenotype switch in CASMCs.
- CagA exposure led to increased cellular calcification and a pro-inflammatory response.
Conclusions:
- H. pylori CagA promotes osteogenic transformation and calcification in CASMCs.
- CagA contributes to vascular calcification through inducing an osteogenic phenotype and inflammation.
- H. pylori infection may play a role in the pathogenesis of vascular calcification via CagA.
Abstract:
Helicobacter pylori (H. pylori) has been associated with cardiovascular diseases. The pro-inflammatory H. pylori virulence factor cytotoxin-associated gene A (CagA) has been detected in serum exosomes of H. pylori-infected subjects and may exert systemic effects throughout the cardiovascular system. The role of H. pylori and CagA in vascular calcification was hitherto unknown. The aim of this study was to determine the vascular effects of CagA through human coronary artery smooth muscle cell (CASMC) osteogenic and pro-inflammatory effector gene expression as well as interleukin 1β secretion and cellular calcification. CagA upregulated bone morphogenic protein 2 (BMP-2) associated with an osteogenic CASMC phenotype switch and induced increased cellular calcification. Furthermore, a pro-inflammatory response was observed. These results support that H. pylori may contribute to vascular calcification through CagA rendering CASMCs osteogenic and inducing calcification.
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