Research Paper Volume 12, Issue 16 pp 16224—16237
SirT3 activates AMPK-related mitochondrial biogenesis and ameliorates sepsis-induced myocardial injury
Figure 2. Overexpression of SirT3 or activation of AMPK attenuates LPS-mediated cardiomyocyte dysfunction. (A–F) Cardiomyocyte contractility in response to LPS treatment. Lentivirus-loaded SirT3 (SirT3-OE) and AMPK agonist (AICAR) were incubated with cardiomyocyte in the presence of LPS. +dL/dt is the maximal velocity of shortening. −dL/dt is the maximal velocity of relengthening. TPS, time to peak shortening; TR90, time to 90% relengthening. *P < 0.05.