Mathematical Biology Seminar
Cardiovascular disease, representing a broad array of pathologies including coronary artery disease, hypertension, and stroke, is the leading cause of death in the United States. Acute myocardial infarction (MI) alone results in an estimated annual incidence of 720,000 new cases, while 335,000 individuals will endure a recurrence. It is widely appreciated that the mitochondrial responses that occur immediately following MI are dynamically regulated by altering mitochondrial form and function. Mitochondria undergo enhanced fission resulting in mitochondria fragmentation. However, the physiological role of mitochondria fragmentation in acute MI is incompletely understood. In the current study, we develop a family of models which track the evolution of the distribution of mitochondrial sizes. In the appropriate asymptotic limit, the model provides a novel method for quantification of changes in relative fission rate from histograms of mitochondria sizes.