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Normal heart function relies of the fine-tuned synchronization of cellular components. In healthy hearts, calcium oscillations and physical contractions are coupled across a synchronised network of 3 billion heart cells. When the process of functional isolation of rogue cells isn’t successful, the network becomes maladapted, resulting in cardiovascular diseases, including heart failure and arrythmia. To advance knowledge on this normal-to-disease transition we must first address the lack of a mechanistic understanding of the plastic readaptation of these networks. In this talk I will explore coupling and loss of synchronisation using a mathematical model of calcium oscillations informed by experimental data. I will show some preliminary results pointing at the heterogeneity hidden behind seemingly uniform cell populations, as a causative mechanism behind disrupted dynamics in maladapted networks.
