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. Author manuscript; available in PMC: 2023 Dec 31.
Published in final edited form as: Biochem Biophys Res Commun. 2022 Nov 13;637:170–180. doi: 10.1016/j.bbrc.2022.11.014

Figure 1. Upregulated SIRT1 exacerbated cardiac dysfunction under pressure overload-induced heart failure (HF).

Figure 1.

(A) The protein and mRNA expression levels of SIRT1 were upregulated in the left ventricles (LV) of Sirt1f/f heart after 6 weeks of transverse aortic constriction (TAC)-induced pressure overload. Biological replicates N=8 for each group. P value was determined by two-way ANOVA with Tukey’s post-hoc test. (B) Echocardiography showed that Sirt1f/f mice were vulnerable to TAC-induced pressure overload, as shown by decreased ejection fraction (EF) and fractional shortening (FS). Left: Representative images of M-mode echocardiography. Right: Quantification of echocardiography measurements for EF and FS. Biological replicates N=8 for each group. P value was determined by two-way ANOVA with Tukey’s post-hoc test. (C) Electrocardiography (ECG) showed that Sirt1f/f mice developed cardiac contractile dysfunction under 6 weeks of post TAC with reduced Q, R, and T amplitudes and prolonged JT and Tpeak-Tend interval. Upper: Representative images of ECG parameters. Lower: Quantification of ECG measurements. Biological replicates N=8 for each group. P value was determined by two-way ANOVA with Tukey’s post-hoc test. Biological replicates N=8 for each group. P value was determined by two-way ANOVA with Tukey’s post-hoc test.