Billions of cells in the body die every day as part of normal cellular turnover and in disease. The removal of dying cells by phagocytes, known as ‘efferocytosis’, is a critical biological process that mantains tissue homeostasis through replenishing dying cells and limiting inflammation.
Our team aims to understand how dying cells within the blood vessels communicate with surrounding tissue and to elucidate the importance of cell clearance by vascular cells, both in the context of normal vessel maintenance and to promote vessel repair following injury or disease. We have a special interest in how vascular cells participate in efferocytosis during inflammatory vascular diseases such as atherosclerosis and hope to identify novel therapeutic targets that may limit plaque progression.
Dr Baxter was shortlisted for an Australian Vascular Biology Society ECR ‘Rising Star’ award in 2023 and was awarded a National Heart Foundation Vanguard Award in 2024 to investigate novel therapeutic targets for atherosclerosis that promote cell clearance.
Research areas
Endothelial cell efferocytosis
‘Efferocytosis’, i.e. the removal of dying cells by special cells termed phagocytes, is a critical process that prevents inflammation and replenishes damaged cells. Impaired efferocytosis is linked to chronic conditions including atherosclerosis and autoimmunity. Although efferocytosis is a well-described function of certain cell types, the role of vascular endothelial cells that line the blood vessels in mediating efferocytosis is currently unknown.
Our team aims to define the mechanisms and functions of efferocytosis by vascular endothelial cells using cell-based methods as well as in vivo transgenic animal models of cell clearance including zebrafish and mouse.
Endothelial cell-derived apoptotic bodies in intercellular communication
During the programmed cell death pathway of ‘apoptosis’, cells undergo a fragmentation process resulting in the formation of large membrane-bound cell fragments termed ‘apoptotic bodies’ (ApoBDs), a type of extracelluar vesicle. ApoBDs are emerging as important mediators of interellular communication through the trafficking of active biomolecules such as lipids, proteins and nucleic acids between cells and tissues within the body.
Using cell-based in vitro methods and mouse models, our team studies the formation of ApoBDs by endothelial cells during vascular inflammation examines the ability of endothelial cell-derived ApoBDs to modulate innate and adaptive immune processes.
Targeting efferocytosis in atherosclerosis
Atherosclerotic plaques that block arteries can lead to life-threatening clinical events such as heart attack and stroke. The removal of dying cells by special cells called phagocytes is a critical process in the body that limits inflammation and promotes tissue repair. During atherosclerosis, dead cell removal is impaired and contributes to plaque growth, although there are currently no treatments that boost dead cell removal in plaques. Our team has recently found that increasing the way cells break apart or ‘fragment’ when they die enhances their ability to be removed by phagocytes.
Using complimentary genetic and pharmacological approaches including a genetic mouse model of enhanced dying cell fragmentation and FDA-approved drugs that promote dying cell fragmentation, our team aims to examine the impact of boosting dead cell removal on plaque growth during atherosclerosis.
Donia Abeid Amy Hodge (co-supervised; primary supervisor Associate Professor Ivan Poon) Dilara Ozkocak (co-supervised; primary supervisor Associate Professor Ivan Poon) Abdulsatar Jamal (co-supervised; primary supervisor Associate Professor Ivan Poon)
