Key result
Increased M1-SIRT3 expression prevented doxorubicin-induced cardiac remodeling and dysfunction in transgenic mice and attenuated superoxide formation in cardiomyocytes.
Why the study?
High doses of doxorubicin put cancer patients at risk for dilated cardiomyopathy, and whether SIRT3 expression can attenuate this toxicity in vivo by preventing mitochondrial protein acetylation was investigated.
Population
Nontransgenic, M3-SIRT3, and M1-SIRT3 transgenic mice, and primary rat and human induced stem cell derived cardiomyocytes
Comparison
M3-SIRT3 or M1-SIRT3 expression vs controls during doxorubicin treatment
Design
Preclinical animal and cellular study
Follow-up
4 weeks
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SIRT3 overexpression should not yet guide cardio-oncology practice; leaves open its role as a target against anthracycline cardiomyopathy.
Mitochondrial-localized SIRT3 (M1-SIRT3) prevents doxorubicin-induced dilated cardiomyopathy and oxidative stress in preclinical models, highlighting a potential therapeutic target.
A 2022 study studied Doxorubicin-induced dilated cardiomyopathy. SIRT3 expression (M1-SIRT3 and M3-SIRT3) vs. Nontransgenic mice and deacetylase deficient mutants was evaluated on Cardiac structure and function and oxidative stress. Increased M1-SIRT3 expression prevented doxorubicin-induced cardiac remodeling and dysfunction in transgenic mice and attenuated superoxide formation in cardiomyocytes.
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