International Partnering Award: Using AI to assess senescence and mitochondrial morphology in calcifying VSMCs
Lead Research Organisation:
University of Edinburgh
Department Name: The Roslin Institute
Abstract
During natural ageing, calcified tissue frequently develops within arteries, the blood vessels that form a network to distribute oxygen-rich blood to the entire body. This process predominantly involves changes in the function of the main type of cell present within the arteries, the vascular smooth muscle cell (VSMC). This is a significant risk factor in the development of future life threatening cardiovascular events, including heart attack and stroke. Identifying new molecules and pathways involved in arterial calcification and novel pharmacological targets that prevent this process could reduce the risk of cardiovascular disease and enhance the quality of life for the elderly.
We have recently published seminal findings revealing, for the first time, that calcifying VSMCs, not only undergo senescence (a process by which a cell ages, changes shape and permanently stops dividing but does not die), but also show longer mitochondria (the energy powerhouses of the cell) which work less efficiently (Phadwal et al., 2023). Present in nearly all types of cells, mitochondria are vital to survival as they generate the energy of the cell. We now ask are our observations simply two parallel consequences of calcification? Or do specific VSMCS first undergo senescence, which then drives mitochondrial elongation within those cells? A more complete understanding of this process will enable our long term ambition to explore the targeting of senescence as a timely and innovative treatment strategy to promote healthy ageing through the inhibition of arterial calcification.
We have recently published seminal findings revealing, for the first time, that calcifying VSMCs, not only undergo senescence (a process by which a cell ages, changes shape and permanently stops dividing but does not die), but also show longer mitochondria (the energy powerhouses of the cell) which work less efficiently (Phadwal et al., 2023). Present in nearly all types of cells, mitochondria are vital to survival as they generate the energy of the cell. We now ask are our observations simply two parallel consequences of calcification? Or do specific VSMCS first undergo senescence, which then drives mitochondrial elongation within those cells? A more complete understanding of this process will enable our long term ambition to explore the targeting of senescence as a timely and innovative treatment strategy to promote healthy ageing through the inhibition of arterial calcification.