FIGURE 4.

FNDC5 protects against aging‐related cardiac dysfunction by activating AMPKα. (a‐b) 6‐month (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 detect AMPKα and downstream acetyl CoA carboxylase (ACC) phosphorylation in murine hearts (n = 6). (c‐d) Western blot images and the statistical results of nucleotide‐binding oligomerization domain‐like receptor with a pyrin domain 3 (NLRP3), apoptosis‐associated speck‐like protein (ASC), and caspase‐1 p20 proteins (n = 6). (e) The caspase‐1 activity in murine hearts (n = 6). (f) Heart weight‐to‐tibia length (HW/TL) in mice (n = 6). (g) Quantification of the cardiomyocyte area in mice (n = 6). (h) Average collagen volume in mice (n = 6). (i) Echocardiographic and hemodynamic parameters of cardiac function in mice, including fractional shortening (FS) and the peak rates of isovolumic pressure development (+dP/dt) in mice (n = 8). (j) The ratio of the early (E) to late (A) ventricular filling velocities (n = 8). Values represent the mean ±standard deviation. *p < 0.05 versus the matched group. NS indicates no significance