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Protective role of Pannexin1 in lymphatic endothelial cells in the progression of atherosclerosis in female mice.
PLoS One
January 2025
Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland.
Atherosclerosis is a progressive arterial disease arising from imbalanced lipid metabolism and a maladaptive immune response. The lymphatic system ensures tissue fluid homeostasis, absorption of dietary fats and trafficking of immune cells to draining lymph nodes, thereby potentially affecting atherogenesis. Endothelial cell-specific deletion of Pannexin1 (Panx1) in apolipoprotein E-deficient (Apoe-/-) mice increased atherosclerosis, suggesting a protective role for Panx1 channels in arterial endothelial function.
View Article and Find Full Text PDFCirculatory microRNAs in acute coronary syndrome: An update.
Kardiol Pol
January 2025
Core Facilities, Medical University of Vienna, Vienna, Austria.
Micro-ribonucleic acids (miRs) are small, non-coding RNAs, which play an important role in atherosclerotic plaque formation, development, and stability. Plaque destabilization and rupture lead to acute coronary syndromes (ACS). Previous studies have implicated several different miRs in the pathogenesis of atherosclerosis.
View Article and Find Full Text PDFPaternal family history of premature atherosclerotic disease and perinatal death: A population-based cohort study.
PLoS One
January 2025
Department of Global Public Health and Primary Care, Faculty of Medicine, University of Bergen, Bergen, Norway.
Background: Studies have reported that pregnancies conceived by fathers with modifiable cardiovascular risk factors are at higher risk of ending in losses compared to those without such risk factors. Our objective was to examine the association between paternal family history _a non-modifiable risk factor_ of premature atherosclerotic disease and perinatal death.
Methods: This is a population-based cohort study.
Background: Vascular endothelial cell-derived exosomes are thought to mediate disease progression by regulating macrophage polarization. However, its mechanism in diabetes mellitus (DM)-related atherosclerosis (AS) progress is unclear.
Methods: High-glucose (HG) and oxLDL were used to induce human cardiac microvascular endothelial cells (HCMECs) to mimic DM-related AS model.
Floralozone attenuates atherosclerotic vascular injury by regulating AMPKα/SREBP-1c pathway and down-regulating miR-33-5p.
Eur J Nutr
January 2025
College of Pharmacy, Sanquan College of Xinxiang Medical University, Xinxiang, 453003, China.
Background: Severe disruption of lipid metabolism in vivo is one of the central mechanisms in the development of atherosclerotic vascular injury (AVI). Reverse cholesterol transport (RCT) plays a pivotal role in eliminating excess cholesterol, preventing lipid deposition in the aorta, and reducing plaque formation associated with AVI. Floralozone (FL) reduces endothelial cell injury in AVI rats by regulating sphingosine-1-phosphate (S1P) expression.
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