Mitochondrial redox regulation in heart failure
Mitochondria are the main supplier of cellular energy in the form of ATP, but also the major source of reactive oxygen species (ROS). The heart consumes large amounts of ATP, and therefore, supply needs to be tightly adjusted to the constantly varying demand. In various forms of heart failure, an energetic mismatch occurs, either through excessive demand or defects in the supply, which can be related to defects in excitation-contraction coupling which compromise mitochondrial calcium uptake required for Krebs cycle activation. Since in mitochondria, the Krebs cycle also regenerates NADPH, which is needed for the detoxification of ROS, such mechanoenergetic uncoupling can increase ROS emission from mitochondria, deteriorating excitation-contraction coupling and causing arrhythmias, cell death and maladaptive remodelling. In my presentation, I will discuss how defects in mechano-energetic coupling contribute to the pathophysiology of heart failure and hereditary cardiomyopathies.
This will be a hybrid seminar; prior registration is required.
Please contact info@sfb1425.uni-freiburg.de.
