Mitochondrial Iron: A Mathematical Model for Iron Regulatory Disease
Friedreich's ataxia (FRDA) is a genetic disease that leads to deficiency in the mitochondrial protein, Frataxin. In turn an accumulation of iron begins to propagate within the mitochondria resulting in cell death by oxidative stress. In this work we present a mechanistic mathematical model that incorporates both cytoplasm and mitochondria key processes responsible for bring iron balance to a healthy cell and iv permanent imbalance in an unhealthy cell. We hope to gain insight into the still unclear biological course of the FRDA within a human cell. Through sensitivity analysis we investigate components that are the most critical to the system and that can lead to effective treatments. Numerical simulations show that the model captures some biological properties necessary to model the role of iron and the interplay of various cellular processes within the cell. Our research seeks to understand and construct a biologically relevant robust model of iron homeostasis that can be used to in silico test the effects of Frataxin deficiency while incorporating both mitochondrial and cytoplasmic iron processes.
- Poster session award recipient at the 2013 AMS/MAA Joint Mathematics Meeting in San Diego, CA
Vanessa Chastain- New College of Florida
Jessica Lunsford- East Tennessee State University
Aaron Ortega- University of Texas at El Paso
Ricardo Reyes Grimaldo- Universidad Autonoma del Estado de Hidalgo
Erika T. Camacho- Arizona State University