This animal study demonstrates that NMN ameliorates type 2 diabetes-induced myocardial fibrosis in mice through upregulation of SIRT3, which deacetylates GSK3β and suppresses Smad3 phosphorylation—key drivers of cardiac fibrosis. The research shows NMN reversed elevated fibrosis markers (collagen I, α-SMA) and improved cardiac function and structure in diabetic mice. This mechanistic work supports NMN’s therapeutic potential as an intervention for diabetes-related cardiac complications, a significant comorbidity concern for practitioners.
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NMN reduced cardiac fibrosis markers in diabetic mice via SIRT3/GSK3β/Smad3; supports monitoring cardiac health in diabetic patients using NMN.