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Sirtuin 1 Activation Mitigates Murine Vasculitis Severity by Promoting Mitophagy.
Asli E Atici1,2, Prasant K Jena1,2, Thacyana T Carvalho1,2
1Department of Pediatrics, Cedars-Sinai Guerin Children's (A.E.A., P.K.J., T.T.C., B.L.R., E.A.A., M.E.L., A.C.G., Y.L., S.C., T.R.C., M.A., M.N.R.), Cedars‑Sinai Health Sciences University, Los Angeles, CA.
Circulation Research
|May 15, 2026
Summary
The nicotinamide adenine dinucleotide-SIRT1 pathway is impaired in Kawasaki disease, leading to cardiovascular inflammation. Boosting SIRT1 can reduce vasculitis and inflammation in this pediatric condition.
Area of Science:
- Cardiovascular Research
- Immunology
- Pediatric Disease
Background:
- SIRT1 (sirtuin 1) is a protein deacetylase involved in cardiovascular inflammation.
- Its role in Kawasaki disease, a pediatric vasculitis causing coronary artery aneurysms, is not well understood.
Purpose of the Study:
- To investigate the role of the nicotinamide adenine dinucleotide (NAD)-SIRT1 axis in the pathogenesis of Kawasaki disease.
- To evaluate the therapeutic potential of targeting SIRT1 in a murine model of the disease.
Main Methods:
- Utilized a Lactobacillus casei cell wall extract (LCWE) murine model of Kawasaki disease.
- Assessed vasculitis severity in mice with altered SIRT1 expression or NAD precursor supplementation.
- Conducted proteomics, echocardiography, immunofluorescence, flow cytometry, and Western blot analyses.
Main Results:
- SIRT1 expression was downregulated in Kawasaki disease lesions, correlating with reduced NAD levels.
- NAD precursor supplementation or SIRT1 overexpression ameliorated LCWE-induced vasculitis.
- SIRT1 deficiency in specific cells exacerbated disease, while its overexpression improved cardiac function and reduced inflammation.
Conclusions:
- An impaired NAD-SIRT1 axis contributes to Kawasaki disease pathogenesis.
- Targeting the NAD-SIRT1 axis shows therapeutic promise for reducing cardiovascular lesions and inflammation in Kawasaki disease.
