NMN reduced myocardial fibrosis in diabetic mice; 3-TYP blocked the effect
In diabetic mice, NMN lessened myocardial interstitial fibrosis and related protein changes; the inhibitor 3-TYP blocked these benefits, supporting a proposed SIRT3-linked mechanism. [1]
Automatic summary · not editorially reviewed
The key findings
The mouse experiment had control, diabetic, diabetic plus NMN and diabetic plus NMN plus 3-TYP groups. [1]
Diabetic mice showed pronounced myocardial interstitial fibrosis and altered cardiac structure and function. [1]
NMN's benefits were inhibited by 3-TYP, and the authors propose a possible SIRT3-linked mechanism. [1]
The source at a glance
- Study type / format
- Preclinical mouse experiment (abstract)
- Population / context
- Mice with type 2 diabetes-induced myocardial fibrosis, plus control mice.
- Summary based on
- Study abstract
- Original publication
- August 10, 2026
Diabetic mice, four groups, fibrosis measured
The abstract describes a mouse experiment with four groups: control, diabetic, diabetic plus NMN, and diabetic plus NMN plus 3-TYP. The researchers measured blood glucose, tibia length, cardiac function, myocardial interstitial fibrosis and reactive oxygen species. They also analysed SIRT3, GSK3β, acetylated GSK3β and downstream fibrosis-related proteins, plus the interaction between SIRT3 and GSK3β.
Supporting source [1]
NMN eased fibrosis; 3-TYP reversed the benefit
Diabetic mice showed pronounced myocardial interstitial fibrosis and altered cardiac structure and function. Levels of acetylated GSK3β relative to GSK3β, phosphorylated Smad3 relative to total Smad3, α-SMA and Collagen I were elevated, while SIRT3 expression was reduced. NMN ameliorated these changes, and 3-TYP effectively inhibited the benefits. The authors propose that NMN may work by raising SIRT3, strengthening its interaction with GSK3β and lowering GSK3β acetylation, ultimately suppressing Smad3 phosphorylation.
Supporting source [1]
Abstract-only mouse evidence, mechanism proposed
This is an abstract of a mouse study; the full text was not reviewed. The mechanism linking SIRT3, GSK3β acetylation and Smad3 phosphorylation is described as possible, not established. The findings concern diabetes-induced myocardial fibrosis in mice and do not show effects on human lifespan or human heart disease.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. This is a mouse study, and the SIRT3–GSK3β–Smad3 mechanism is proposed, not established. No human outcomes are reported.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Ma Z, Yao L, Zhang K, Yang Y. · europepmc.org · August 10, 2026