Well-posedness of a mathematical model of diabetic atherosclerosis

Abstract

Atherosclerosis is a leading cause of death in the United States and worldwide; it emerges as a result of multiple dynamical cell processes including hemodynamics, endothelial damage, innate immunity and sterol biochemistry. Making matters worse, nearly 21 million Americans have diabetes, a disease where patients' cells cannot efficiently take in dietary sugar, causing it to build up in the blood. In part because diabetes increases atherosclerosis-related inflammation, diabetic patients are twice as likely to have a heart attack or stroke. Past work has shown that hyperglycemia and insulin resistance alter function of multiple cell types, including endothelium, smooth muscle cells and platelets, indicating the extent of vascular disarray in this disease. Although the pathophysiology of diabetic vascular disease is generally understood, there is no mathematical model to date that includes the effect of diabetes on plaque growth. In this paper, we propose a mathematical model for diabetic atherosclerosis; the model is given by a system of partial differential equations with a free boundary. We establish local existence and uniqueness of solution to the model. The methodology is to use Hanzawa transformation to reduce the free boundary to a fixed boundary and reduce the system of partial differential equations to an abstract evolution equation in Banach spaces, and apply the theory of analytic semigroup.