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Here, we show that high fat consumption in mice leads to the accumulation of lipid droplets in endothelial cells throughout the organism and that lipid droplet accumulation in endothelium suppresses endothelial nitric oxide synthase (eNOS), reduces NO production, elevates blood pressure, and accelerates atherosclerosis.
Our analyses suggest the interferon-γ–inducible chemokine CXCL10 to be a potentially causal mediator for atherosclerosis in 3 vascular compartments and, as such, could serve as a promising drug target for atheroprotection.
However, the role of METTL4-mediated mitoepigenetic regulation in atherosclerosis is still unknown. We explored the mechanism of METTL4 involvement in atherosclerosis usingMettl4Mac-KO-Apoe-/-andMettl4MUT-Apoe-/-mice and cell models, as well as bone marrow transplantation.
The EGFR (epidermal growth factor receptor) has been shown to mediate inflammatory vascular diseases, including atherosclerosis and aortic aneurysm. Pharmacological inhibition of EGFR or downstream ER stress may be a promising therapeutic strategy for preventing aneurysm rupture and subarachnoid hemorrhage.
Such fibrils are associated with major human diseases including Alzheimer’s and Parkinson’s diseases, diabetes, and heart diseases such as atherosclerosis and calcific aortic valve disease. “We
This modification will affect not only the onset of diabetes but also the related onset of atherosclerosis. Therefore, in this review, based on the whole process of atherosclerosis evolution, we explored the possible existence of acetylation/deacetylation caused by diabetes.
Nevertheless, the correlation between ISNA and the progression of untreated coronary segments affected by native atherosclerosis remains incompletely investigated. Nevertheless, the correlation between ISNA and the progression of untreated coronary segments affected by native atherosclerosis remains incompletely investigated.
1,6 Until recently atherosclerosis has been thought of as the result of passive lipid accumulation in the vessel wall. However, the development of atherosclerosis is now known to be much more complex, with a key role for immune cells and inflammation in conjunction with hyperlipidemia and elevated LDL levels.7 Curr Opin Lipidol.
Statins are the primary drugs for treating hyperlipidemia or atherosclerosis, yet some patients remain unresponsive to them, and pregnant women are prohibited from taking statins. IntroductionThe incidence of metabolic disorders during pregnancy is increasing year by year, with diseases including hypertension and hyperlipidemia.
Keynote speaker and atherosclerosis expert Peter Libby, MD , captivated the audience with an update on his research into inflammation and atherosclerosis. He discussed therapeutic options not only for treating atherosclerosis but also for preventing cardiovascular disease. Experts like Louis J.
Aortic diseases such as atherosclerosis, aortic aneurysms, and aortic stiffening are significant complications that can have significant impact on end-stage cardiovascular disease. Hypertension, Ahead of Print.
The complex development of atherosclerosis manifests as intimal plaque which occurs in the presence or absence of traditional risk factors. Atherosclerotic coronary artery disease (CAD) is the causal pathological process driving most major adverse cardiovascular events (MACE) worldwide.
Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis: a randomized controlled trial. Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: the ASTEROID trial. 2004 Mar 3;291(9):1071-80. 4 ASTEROID Investigators. 2006 Apr 5;295(13):1556-65.
PAD is a serious, progressive cardiovascular disease primarily caused by a buildup of fatty plaque in the blood vessels, or atherosclerosis. Pharmacological and behavioral-based strategies often increase the smoking cessation rate in people with PAD, however, these strategies are underused.
Atherosclerosis is an insidious and progressive inflammatory disease characterized by the formation of lipid-laden plaques within the intima of arterial walls with potentially devastating consequences.
Dysregulation of the innate and adaptive immune system is accelerated by CKD and results in increased systemic inflammation, a heightened local vascular inflammatory response leading to accelerated atherosclerosis, and dysfunction of the cardiac and renal endothelium and microcirculation.
His main career interests are in improving treatments for patients with intracranial arterial atherosclerosis and helping to mentor the next generation of clinical and translational scientists. The Ralph L. Raed Joundi, M.D., is the Vascular Cognitive Impairment Award recipient.
Then, we collected literature-validated TMYXP blood component targets for further network pharmacology analysis.ResultsAll blood components of TMYXP exhibited non-toxic properties. This study focused on peripheral blood mononuclear cell samples from 6 elderly patients with CHD over 60 years old (GSE142008).
Analysis indicated that the 9 hub genes (AKT1, HSP90AA1, SRC, GSK3, VEGFR2, RHOA, ENO1, PKM, and IL-2) play roles in MF treatment by participating in signaling pathways related to prostate cancer, lipid and atherosclerosis, and insulin resistance.
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