Numerous mitochondrial defects have been present in the mouse model of Pompe condition, such as mitochondrial calcium extra, increased reactive oxygen species, decreased mitochondrial membrane potential, and reduced oxygen consumption and ATP production (Lim et al (2015) A murine Niemann‐Decide on C1 I1061T knock‐in model recapitulates the pathological characteristics of https://jasperujwit.activoblog.com/28984338/lsds-options