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| http://dx.doi.org/10.1161/CIRCIMAGING.117.006533 | DOI Listing |
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Effect of Monosodium Urate Crystal Deposition on Atherosclerotic Carotid Plaques.
J Clin Med
January 2025
Departments of Neurosurgery, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
The accumulation of uric acid in arteriosclerotic plaques has recently attracted attention. Because the interaction between hyperuricemia and atherosclerosis is complex, the details remain obscure. We aimed to elucidate the clinical effect of monosodium urate monohydrate (MSU) deposition on carotid plaques.
View Article and Find Full Text PDFCarotid artery atherosclerotic stenosis is an important annual cause of stroke in the United States. Moreover, the incidence of carotid artery stenosis is significantly increasing due to the widespread popularity of high fat and high salt diets, sedentary lifestyles, and the increasing age of the population. Of major importance to cardiovascular specialists is the fact that individuals with atherosclerotic carotid artery stenosis can have a prevalence of atherosclerotic coronary artery disease as high as 50 to 75%.
View Article and Find Full Text PDFApplication of adipose tissue-derived stem cell therapy with a clinically relevant dose does not significantly affect atherosclerotic plaque characteristics in a streptozotocin-induced hyperglycaemia mouse model.
J Mol Cell Cardiol Plus
September 2024
Department of Pathology, Amsterdam University Medical Centres (AUMC), Location VUmc, Amsterdam, the Netherlands.
Aims: Diabetes mellitus (DM) induces increased inflammation of atherosclerotic plaques, resulting in elevated plaque instability. Mesenchymal stem cell (MSC) therapy was shown to decrease plaque size and increase stability in non-DM animal models. We now studied the effect of MSC therapy in a streptozotocin-induced hyperglycaemia mouse model using a clinically relevant dose of adipose tissue-derived MSCs (ASCs).
View Article and Find Full Text PDFMelatonin stabilizes atherosclerotic plaques: an association that should be clinically exploited.
Front Med (Lausanne)
December 2024
CENECON, Faculty of Medical Sciences, Universidad de Buenos Aires, and Pontificia Universidad Catolica Argentina, Buenos Aires, Argentina.
Atherosclerosis is the underlying factor in the premature death of millions of humans annually. The cause of death is often a result of the rupture of an atherosclerotic plaque followed by the discharge of the associated molecular debris into the vessel lumen which occludes the artery leading to ischemia of downstream tissue and to morbidity or mortality of the individual. This is most serious when it occurs in the heart (heart attack) or brain (stroke).
View Article and Find Full Text PDFBlack phosphorus nanoplatform coated with platelet membrane improves inhibition of atherosclerosis progression through macrophage targeting and efferocytosis.
Acta Biomater
January 2025
Department of Radiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. Electronic address:
Plaque rupture in atherosclerosis (AS) is a major cause of acute cardiovascular events. Macrophage-induced inflammatory responses and accumulation of excess reactive oxygen species (ROS) primarily induce unstable plaques. Therefore, targeting ROS clearance and functional modulation of macrophages are clinically crucial for improving plaque stability and inhibiting AS progression.
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