Endothelial LOX-1 activation differentially regulates arterial thrombus formation depending on oxLDL levels: role of the Oct-1/SIRT1 and ERK1/2 pathways
ConclusionsThus, LOX-1 differentially regulates thrombus formation in vivo depending on the degree of activation by oxLDL. At low oxLDL levels LOX-1 activates the protective Oct-1/SIRT1 pathway, while at higher levels of the lipoprotein switches to the thrombogenic ERK1/2 pathway. These findings may be important for arterial thrombus formation in ACS and suggest that SIRT1 may represent a novel therapeutic target in this context.
CONCLUSIONS: Elevated levels of sdLDL-C were associated with a higher prevalence of AIS, especially in non-cardioembolic stroke subtypes. After adjustment for other risk factors, sdLDL-C was found to be an independent risk factor for AIS. Also, sdLDL-C level was strongly associated with AIS severity and poor functional outcomes. Logistic regression models for AIS risk and prognosis prediction were established to help clinicians provide better prevention for high-risk subjects and monitor their prognosis. PMID: 32062644 [PubMed - as supplied by publisher]
An 85-year-old man presented with left hemiparesis, too late for any intervention. Brain computed tomography (CT) revealed a right hemispheric infarct. He had a history of diabetes mellitus (on metformin, statin), hypertension (on losartan/lercanidipine), past smoking, COPD (on inhalers) and peripheral artery disease (on aspirin).
Authors: Alwi I Abstract Over more than two decades, the concept of atherosclerosis has developed and lead to inflammatory hypothesis. Inflammation plays an important role on pathogenesis of atherothrombosis and coronary heart disease (CHD), including acute coronary syndrome (ACS). Although the management of ACS has been demonstrated to be beneficial for secondary prevention of coronary heart disease (such as using statin and aspirin) and also seemed to have positive effect on inflammation, the identification of effective management, specifically targeting inflammation, has been not been comprehensively understood....
ConclusionsApplied immediately after stent implantation, a ML model better differentiates those patients who will present SR over current discriminators.
In conclusion, Nar improves the function of HUVECs under HG/HF stress through activating the PI3K-Akt-mTOR pathway to inhibit autophagy. The findings offer an insight into HG/HF stress-induced autophagy and indicate that Nar might have potential to prevent and treat the diabetic angiopathy. PMID: 32045600 [PubMed - as supplied by publisher]
CONCLUSIONS: The Suita CVD risk model is feasible to use and improves predictability of the incidence of CVD relative to the FRS model in Japan. PMID: 32023562 [PubMed - as supplied by publisher]
Abstract Atherosclerosis is a vascular disease responsible for acute heart attacks and stroke, which are leading causes of death not only in industrialized countries but also worldwide, and the number of patients afflicted by this disease has been increasing in Japan. High-density lipoprotein (HDL) is the plasma lipoprotein that carries what is often called your "good cholesterol" through the blood. This good cholesterol moniker is associated with HDL because higher circulating levels of this lipoprotein are associated with a well-known reduction in the risk of arteriosclerosis. Moreover, many protective...
CONCLUSIONS: Low EPA/AA ratio at baseline and treatment without statins could predict mortality, recurrent ischemic stroke, cardiovascular and peripheral artery diseases, and hemorrhagic stroke among patients with acute ischemic stroke. The combination of baseline EPA/AA ratio and statin therapy could be critical in predicting the long-term prognosis of ischemic stroke patients. PMID: 31969533 [PubMed - as supplied by publisher]
Conclusion: LT for children with PA is a viable treatment option with acceptable outcomes.
CONCLUSIONS: We have shown that disruption of PLTP-mediated HDL maturation reduces SR-BI deficiency-driven atherosclerosis susceptibility in mice despite the induction of proatherogenic metabolic complications in the double knockout mice. PMID: 31941380 [PubMed - as supplied by publisher]