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Updated: May 5, 2026
Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
Colchicine Inhibits Smooth Muscle Cell Phenotypic Switch and Aortic Dissection in Mice-Brief Report
Hui Jiang1,2, Yaping Zhao1,3, Mei Jin4
1Department of Endocrinology, Centre for Leading Medicine and Advanced Technologies of IHM, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei (H.J., Y.Z., Z.Z., J.W., S.X.).
Background:
Aortic dissection (AD) is a severe cardiovascular disorder characterized by intimal tearing and subsequent delamination of the aortic wall. The pathogenesis of AD primarily involves the phenotypic switch of vascular smooth muscle cells (VSMCs), degradation of the extracellular matrix, and chronic vascular inflammation. Colchicine, an alkaloid derived from Colchicum autumnale L, is a Food and Drug Administration-approved anti-inflammatory drug with established therapeutic applications in cardiovascular diseases. However, its potential role in modulating the development or progression of AD remains largely unexplored.
Methods:
To investigate the effects of colchicine on AD, a β-aminopropionitrile-induced AD mouse model was used. Colchicine was administered via oral gavage over a 3-week period to evaluate its impact on the incidence and mortality of AD in male C57BL/6J mice. Transcriptome sequencing was performed to identify genes and signaling pathways regulated by colchicine. Additionally, in vitro experiments using primary rat VSMCs were conducted to elucidate the mechanisms underlying colchicine-mediated regulation of VSMC phenotypic switch.
Results:
Colchicine demonstrated a protective effect against AD by attenuating vascular inflammation and suppressing VSMC phenotypic switch. Mechanistically, colchicine reverses VSMC phenotypic switch at least partially by modulating the expression of myocardin, a key regulator of VSMC contractile phenotype. Transcriptomic analysis further revealed specific genes and pathways influenced by colchicine, providing insights into its molecular mechanisms of action.
Conclusions:
This study identifies colchicine as a potential therapeutic drug for AD, highlighting its ability to mitigate hallmark pathological processes such as vascular inflammation and VSMC phenotypic switch. These findings offer a foundation base for the repurposed clinical application of colchicine in AD, which warrants further clinical investigation.
Insights
Colchicine shows protective effects against aortic dissection (AD) by reducing inflammation and vascular smooth muscle cell (VSMC) changes. This suggests colchicine as a potential therapeutic for AD.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Molecular Biology
Background:
- Aortic dissection (AD) is a severe cardiovascular condition involving intimal tearing and aortic wall delamination.
- Key factors in AD pathogenesis include VSMC phenotypic switch, extracellular matrix degradation, and chronic inflammation.
- Colchicine, an anti-inflammatory drug, has known cardiovascular applications but its role in AD is unexplored.
Purpose of the Study:
- To investigate the therapeutic potential of colchicine in preventing and treating aortic dissection.
- To elucidate the molecular mechanisms by which colchicine affects AD pathogenesis, particularly VSMC behavior.
Main Methods:
- A β-aminopropionitrile-induced AD mouse model was used to assess colchicine's impact on AD incidence and mortality.
- Transcriptome sequencing identified genes and pathways regulated by colchicine.
- In vitro studies with primary rat VSMCs explored colchicine's effect on VSMC phenotypic switch.
Main Results:
- Colchicine demonstrated a protective effect in AD, reducing vascular inflammation and suppressing VSMC phenotypic switch.
- Colchicine was found to reverse VSMC phenotypic switch, partly by modulating myocardin expression.
- Transcriptomic analysis provided insights into colchicine's molecular mechanisms in AD.
Conclusions:
- Colchicine shows promise as a therapeutic agent for aortic dissection.
- It mitigates key pathological processes in AD, including vascular inflammation and VSMC phenotypic switch.
- Further clinical investigation is warranted for repurposing colchicine in AD treatment.
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