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Long-Term Treatment of Azathioprine in Rats Induces Vessel Mineralization
Mirjam Schuchardt1, Jaqueline Herrmann1,2, Cornelia Henkel1
1Department of Nephrology and Medical Intensive Care, Charité-Universitätsmedizin Berlin, 12203 Berlin, Germany.
Biomedicines
|April 3, 2021
Summary
Azathioprine (AZA) medication can induce medial vascular calcification (mVC) by increasing calcium in aortic tissue. This occurs via oxidative stress and inflammation, potentially involving the NLRP3 inflammasome pathway.
Area of Science:
- Cardiovascular Research
- Nephrology
- Pharmacology
Background:
- Medial vascular calcification (mVC) is linked to cardiovascular disease, particularly in chronic kidney disease (CKD) patients.
- Increased cardiovascular mortality persists post-kidney transplantation, with immunosuppressants like azathioprine (AZA) suspected to play a role.
Purpose of the Study:
- To investigate the in vivo effects of azathioprine (AZA) on medial vascular calcification (mVC).
- To elucidate the underlying pathophysiological mechanisms of AZA-induced vascular calcification.
Main Methods:
- An in vivo rat model was treated with AZA for 24 weeks.
- Calcium content in aortic tissue was measured.
- Systemic and aortic tissue levels of proinflammatory cytokines (IL-1ß, IL-6) were assessed.
- Expression of VSMC calcification markers and NLRP3 inflammasome activation was evaluated.
Main Results:
- AZA treatment significantly increased calcium content in rat aortic tissue.
- AZA induced oxidative stress and elevated proinflammatory cytokines (IL-1ß, IL-6).
- Vascular smooth muscle cells (VSMCs) showed increased expression of calcification markers.
- The calcification effect was reduced in NLRP3 knockout aortic rings, suggesting pathway involvement.
Conclusions:
- Azathioprine (AZA) administration in vivo induces medial vascular calcification (mVC) in rats.
- The mechanism involves AZA catabolism, oxidative stress, inflammation, and potentially the NLRP3 inflammasome.
- These findings highlight potential vascular risks associated with AZA treatment, warranting further human studies.
