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. 2023 Oct 4;6(12):e202302116. doi: 10.26508/lsa.202302116

Figure 1. Nicotinamide mononucleotide (NMN) administration improves cardiac dysfunction in p32cKO mice.

Figure 1.

(A) Relative mRNA expression levels of the cardiomyopathy biomarkers atrial natriuretic factor and β-myosin heavy chain in the heart. WT and p32cKO mice were treated with or without NMN from 2 to 9 mo of age (WT: n = 4, WT + NMN: n = 6, p32cKO: n = 5, p32cKO + NMN: n = 4). ***P < 0.0001, *P = 0.0302. (B) Cardiac fibrosis as shown by Masson’s trichrome staining for WT and p32cKO mice treated from 2 to 9 mo of age with NMN (n = 3). Eight images were taken for each mouse and the proportions of blue-stained areas were plotted (20 locations in total). Quantification is shown in the right panel. Scale bars, 20 μm. ***P = 0.0001, **P = 0.0043, *P = 0.0152. (C) Metabolite analysis of dopamine and epinephrine in the heart of WT and p32cKO mice treated with NMN from 2 to 9 mo of age (WT, p32cKO, and p32cKO + NMN: n = 5, WT + NMN: n = 6). (D) Kaplan–Meier survival curve for p32cKO mice treated with or without NMN (p32cKO: n = 34, p32cKO+NMN: n = 14) (***P = 0.0005) were analyzed by the log-rank test (**P = 0.0016). (A, B, C) Error bars show the mean ± SD. Data were analyzed by one-way analysis of variance with Tukey’s multiple comparisons test. *P < 0.05, **P < 0.01, ***P < 0.001.