Mathematical Modelling of the Mechanobiology of Arterial Plaque Growth. Plaque growth is a chronic inflammatory response induced by the interactions between endothelial cells, lipids, monocytes/macrophages, smooth muscle cells and platelets in the arteries. It involves many different biological processes, such as lipid deposition, inflammation and angiogenesis, and their interactions with the microcirculation. To understand the underlying mechanobiology, we propose to develop a mathematical mode ....Mathematical Modelling of the Mechanobiology of Arterial Plaque Growth. Plaque growth is a chronic inflammatory response induced by the interactions between endothelial cells, lipids, monocytes/macrophages, smooth muscle cells and platelets in the arteries. It involves many different biological processes, such as lipid deposition, inflammation and angiogenesis, and their interactions with the microcirculation. To understand the underlying mechanobiology, we propose to develop a mathematical model to interpret plaque growth by integrating these dynamic biological processes. It will offer a systematic rational understanding of plaque growth. New models will be provided to better interpret biological data and contribute to our knowledge in quantifying complex biological mechanisms during growth and development.Read moreRead less
Understanding how an old heart gets stiff. Aging is accompanied by a stiffening of the heart and reduced function, which is accelerated by cardiovascular disease and leads to heart failure. How the heart stiffens is poorly understood. A new mechanism is proposed here, involving structural membrane proteins (termed caveolae and cavins) and a signalling molecule (nitric oxide). The current research aims to unravel the interplay between cardiac cells and these proteins/signals to cause stiffness an ....Understanding how an old heart gets stiff. Aging is accompanied by a stiffening of the heart and reduced function, which is accelerated by cardiovascular disease and leads to heart failure. How the heart stiffens is poorly understood. A new mechanism is proposed here, involving structural membrane proteins (termed caveolae and cavins) and a signalling molecule (nitric oxide). The current research aims to unravel the interplay between cardiac cells and these proteins/signals to cause stiffness and to determine whether this process governs normal aging of the heart. This work will advance understanding of how heart function is determined and reveal how the human heart changes with normal aging. Read moreRead less