Publications by authors named "Katie C Y Lee"
Inflammation and a metabolic shift from oxidative metabolism to glycolysis are common in the ischemic heart, the latter partly controlled by pyruvate kinase (muscle, PKM). We previously identified alternative splicing promoting the PKM2 isoform after myocardial infarction (MI). We examined the role of PKM2 physiological upregulation after MI, modeled by ligation of the left anterior descending coronary artery, using global PKM2 knockout (PKM2) mice.
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- Cardiac metabolism primarily uses fatty acids for ATP production in healthy states, shifting to glucose in disease; pyruvate kinase muscle (PKM) isoforms, particularly PKM1 and PKM2, play significant roles in this process.
- Research on PKM2 knockout mice showed decreased glucose levels, reduced ATP content, and impaired mitochondrial function, alongside an increase in reactive oxygen species (ROS) in cardiomyocytes.
- Despite these metabolic disruptions, PKM2 hearts preserved their ejection fraction, suggesting PKM2 helps maintain ATP levels and manage oxidative stress, although its absence may increase vulnerability to stress or injury.