Does electron transport chain dysfunction in neonatal pressure-overload hypertrophy precede cardiomyocyte apoptosis independent of oxidative stress?
In pressure-overload hypertrophy, the transition from compensated left ventricular hypertrophy to failure and cardiomyocyte apoptosis is preceded by mitochondrial complex I and II dysfunction followed by an increase in Bax/Bcl-2 ratios. The mechanism of apoptosis initiation is independent of increased oxidative stress.
da Vinci-assisted laparoscopic right hemicolectomy using a MtL dissection technique achieves similar outcomes as a LtM dissection approach.