Microsocopic Images acquired in the 1st and the 2nd screening

The accumulation of damaged mitochondria in the heart is associated with
heart failure. Mitophagy is an autophagic degradation system that
specifically targets damaged mitochondria. We previously reported
that Bcl2-like protein 13 (Bcl2-L-13) mediates mitophagy and
mitochondrial fission in mammalian cells. However, the in vivo
function of Bcl2-L-13 remains unclear. Here, we demonstrate that
Bcl2-L-13-deficient mice and knock-in mice, in which the phosphorylation
site (Ser272) on Bcl2-L-13 was changed to Ala, showed left ventricular
dysfunction in response to pressure overload. Attenuation of
mitochondrial fission and mitophagy led to impairment of
ATP production in these mouse hearts. In addition, we identified
AMPKα2 as the kinase responsible for the phosphorylation of
Bcl2-L-13 at Ser272. These results indicate that Bcl2-L-13 and
its phosphorylation play an important role in maintaining
cardiac function. Furthermore, the amplitude of stress-stimulated
mitophagic activity could be modulated by AMPKα2.