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Targeted MRI
Published in Robert J. Gropler, David K. Glover, Albert J. Sinusas, Heinrich Taegtmeyer, Cardiovascular Molecular Imaging, 2007
Susan B. Yeon, Andrea J. Wiethoff, Warren J. Manning, Elmar Spuentrup, Rene M. Botnar
Vascular inflammation and associated endothelial activation is believed to play an integral role in initiation and progression of atherosclerosis. Endothelial activation is characterized by the upregulation of leukocyte adhesion molecules such as E- and P-selectin, which facilitate adhesion and migration of monocytes. Differentiation of monocytes into macrophages and subsequent digestion of lipoproteins by macrophages occur in a later stage and eventually lead to the accumulation of lipid filled macrophages, which are believed to be a precursor of rupture-prone vulnerable plaque.
Centralized Endothelial Mechanobiology, Endothelial Dysfunction, and Atherosclerosis
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
Ian Chandler Harding, Eno Essien Ebong
Initially, the development of atherosclerosis was thought of as a passive process of cell proliferation, particularly of smooth muscle cells, and lipid deposition in the form of cholesterol [8]. However, it is now recognized that inflammation plays a large role in the initiation and progression of the disease. Development of atherosclerosis is believed to begin as a result of endothelial activation and dysfunction in combination with low-density lipoprotein (LDL) uptake and retention in the intima [9,10]. The activation and dysfunction of the endothelium is characterized by numerous changes in cell phenotype, including decreased nitric oxide (NO) production, increased cell adhesion receptor expression, increased oxidative stress, and the expression of pro-inflammatory transcription factors [9,10]. Of these changes, decreased bioavailability of NO has been shown to play an exceedingly important role in EC dysfunction [11,12]. The combination of a dysfunctional or pro-atherosclerotic endothelium with the retention of nonmodified and oxidized LDLs leads to the recruitment, adhesion, and accumulation of monocytes within endothelium [9,13–15]. Once in the subendothelial tissue, monocyte-derived macrophages internalize retained LDLs in an attempt to remove them from the surrounding tissue; however, these macrophages fail to clear LDLs from the subendothelial space and instead turn into foam cells, lipid-laden macrophages [9,10,14,15]. This process further stimulates a pro-inflammatory response, which results in increased monocyte proliferation and apoptosis, increased smooth muscle cell proliferation and migration, and eventual formation of an atherogenic plaque [9,15]. The formation and growth of this plaque, however, is actually relatively harmless. Instead, it is the destabilization and rupture of the plaque that poses the potential risk of thrombosis, which can lead to myocardial infarctions and strokes [9,16].
Short-term exercise training reduces glycaemic variability and lowers circulating endothelial microparticles in overweight and obese women at elevated risk of type 2 diabetes
Published in European Journal of Sport Science, 2019
Hossein Rafiei, Emily Robinson, Julianne Barry, Mary Elizabeth Jung, Jonathan Peter Little
Impaired glucose tolerance and the resulting postprandial hyperglycaemic excursions are linked to increased risk of CVD, which is mechanistically linked to endothelial dysfunction. Endothelial microparticles (EMPs) are emerging as circulating biomarkers of endothelial cell damage and dysfunction. Plasma EMPs can be measured by flow cytometry and based on the expression of surface proteins from their parent endothelial cells can provide insight into endothelial cell phenotype. CD31+ EMPs are thought to reflect endothelial cell apoptosis whereas CD62E+ EMPs are characterized by increased inflammation and endothelial activation (Deng, Wang, & Zhang, 2016). Although EMPs can have both negative and positive effects on the endothelium (Berezin, Zulli, Kerrigan, Petrovic, & Kruzliak, 2015), accumulating evidence has indicated that exercise training results in reductions in EMPs in overweight/obese individuals concomitant with an improvement in overall cardiometabolic health (Babbitt et al., 2013). Whether this is linked to improved glucose control and/or alleviation of endothelial damage induced by hyperglycaemic spikes is not known.