FIGURE 1.

FNDC5 attenuates aging‐related cardiac dysfunction in mice. (a) The serum irisin level in 8‐month (M)‐old young and 20‐M‐old aging mice was detected by an ELISA kit (n = 6). (b) FNDC5 protein levels in heart samples from 8‐M‐old young and 20‐M‐old aging mice (n = 6). (c) 6‐M‐old young and 18‐M‐old aging mice were injected with AAV9‐FNDC5 (1 × 10¹¹ viral genome per mouse) from the tail vein for 8 weeks to specifically overexpress FNDC5 in the myocardium or AAV9‐NC as a control, and then, Western blot was performed to identify the efficiency of AAV9‐FNDC5 in young (8‐M‐old) and aging (20‐M‐old) mice (n = 6). (d) Fractional shortening (FS), and left ventricular internal dimension at end‐diastole (LVIDd) or end‐systole (LVIDs) of mice were determined by echocardiography (n = 8). (e) The peak rates of isovolumic pressure development (+dP/dt) of mice (n = 8). (f) The ratio of the early (E) to late (A) ventricular filling velocities (n = 8). (g) Representative pictures of SA β‐gal‐stained heart sections and quantitative results (n = 6). (h) Relative telomere length in murine hearts (n = 6). (i) Cardiac lipofuscin content in murine hearts (n = 6). (j‐k) Western blot images of p16, p19, and p21, and the statistical results (n = 6). Values represent the mean ±standard deviation. *p < 0.05 versus the matched group