Cellular nitric oxide synthesis is affected by disorders in the interdependent $Ca^{2+}$ and $IP_{3}$ dynamics during cystic fibrosis disease

Calcium (\(Ca^{2+}\)), inositol trisphosphate (\(IP_3\)), and nitric oxide (NO) signaling are essential to maintain the structural integrity and physiological activity of fibroblast cells. The accumulation of excess quantity of NO for longer periods can lead to a variety of fibrotic disorders, including heart disease, penile fibrosis in Peyronie’s disease (PD), and cystic fibrosis. The dynamics of these three signaling processes and their interdependence in fibroblast cells are not clearly known to date. A systems biology model is proposed using reaction-diffusion equations for calcium, \(IP_3\), and calcium-dependent NO synthesis in fibroblast cells. The finite element method (FEM) is used to examine \(Ca^{2+}\), \(IP_3\), and NO regulation and dysregulation in cells. The results throw light on the conditions that disturb the coupled \(Ca^{2+}\) and \(IP_3\) dynamics and the influence of these factors on the levels of NO concentration in the fibroblast cell. The findings suggest that changes in source inflow, buffers, and diffusion coefficient might induce an increase or reduction in nitric oxide and \(IP_3\) synthesis, resulting in fibroblast cell diseases. Furthermore, the findings provide new information regarding the size and intensity of diseases in response to changes in several factors of their dynamics, which has been linked to the development of cystic fibrosis and cancer. This knowledge could be valuable for developing novel approaches to the diagnosis of diseases and therapies for various disorders of fibroblast cells.