Blood Lipoproteins Shape the Phenotype and Lipid Content of Early Atherosclerotic Lesion Macrophages: A Dual-Structured Mathematical Model.

Macrophages in atherosclerotic lesions exhibit a spectrum of behaviours or phenotypes. The phenotypic distribution of monocyte-derived macrophages (MDMs), its correlation with MDM lipid content, and relation to blood lipoprotein densities are not well understood. Of particular interest is the balance between low density lipoproteins (LDL) and high density lipoproteins (HDL), which carry bad and good cholesterol respectively.

A Lipid-Structured Model of Atherosclerosis with Macrophage Proliferation.

Atherosclerotic plaques are fatty deposits that form in the walls of major arteries and are one of the major causes of heart attacks and strokes. Macrophages are the main immune cells in plaques and macrophage dynamics influence whether plaques grow or regress. Macrophage proliferation is a key process in atherosclerosis, particularly in the development of mid-stage plaques, but very few mathematical models include proliferation.

A Lipid-Structured Model of Atherosclerotic Plaque Macrophages with Lipid-Dependent Kinetics.

Atherosclerotic plaques are fatty growths in artery walls that cause heart attacks and strokes. Plaque formation is driven by macrophages that are recruited to the artery wall. These cells consume and remove blood-derived lipids, such as modified low-density lipoprotein.

A multiphase model of growth factor-regulated atherosclerotic cap formation.

Atherosclerosis is characterised by the growth of fatty plaques in the inner artery wall. In mature plaques, vascular smooth muscle cells (SMCs) are recruited from adjacent tissue to deposit a collagenous cap over the fatty plaque core. This cap isolates the thrombogenic plaque content from the bloodstream and prevents the clotting cascade that leads to myocardial infarction or stroke.

A two-phase model of early fibrous cap formation in atherosclerosis.

Atherosclerotic plaque growth is characterised by chronic, non-resolving inflammation that promotes the accumulation of cellular debris and extracellular fat in the inner artery wall. This material is highly thrombogenic, and plaque rupture can lead to the formation of blood clots that occlude major arteries and cause myocardial infarction or stroke. In advanced plaques, vascular smooth muscle cells (SMCs) are recruited from deeper in the artery wall to synthesise a cap of fibrous tissue that stabilises the plaque and sequesters the thrombogenic plaque content from the bloodstream.

Dynamics of angiogenesis during wound healing: a coupled in vivo and in silico study.

Objective: The most critical determinant of restoration of tissue structure during wound healing is the re-establishment of a functional vasculature, which largely occurs via angiogenesis, specifically endothelial sprouting from the pre-existing vasculature.

Materials And Methods: We used confocal microscopy to capture sequential images of perfused vascular segments within the injured panniculus carnosus muscle in the mouse dorsal skin-fold window chamber to quantify a range of microcirculatory parameters during the first nine days of healing. This data was used to inform a mathematical model of sequential growth of the vascular plexus.