about
Mechanism of triglyceride lowering in mice expressing human apolipoprotein A5MiR-486 and miR-92a Identified in Circulating HDL Discriminate between Stable and Vulnerable Coronary Artery Disease Patients.Hyperglycemia Determines Increased Specific MicroRNAs Levels in Sera and HDL of Acute Coronary Syndrome Patients and Stimulates MicroRNAs Production in Human Macrophages.Microparticles of healthy origins improve endothelial progenitor cell dysfunction via microRNA transfer in an atherosclerotic hamster model.HDL inhibits endoplasmic reticulum stress by stimulating apoE and CETP secretion from lipid-loaded macrophages.Dysfunctional high-density lipoproteins have distinct composition, diminished anti-inflammatory potential and discriminate acute coronary syndrome from stable coronary artery disease patients.Caffeic acid attenuates the inflammatory stress induced by glycated LDL in human endothelial cells by mechanisms involving inhibition of AGE-receptor, oxidative, and endoplasmic reticulum stress.Homozygous familial hypercholesterolemia: specific indication for domino liver transplantation.Analysis of circulating microRNAs that are specifically increased in hyperlipidemic and/or hyperglycemic sera.Hyperlipidemia-induced hepatic and small intestine ER stress and decreased paraoxonase 1 expression and activity is associated with HDL dysfunction in Syrian hamsters.Inhibition of miR-486 and miR-92a decreases liver and plasma cholesterol levels by modulating lipid-related genes in hyperlipidemic hamstersHyperlipidemia Determines Dysfunctional HDL Production and Impedes Cholesterol Efflux in the Small Intestine: Alleviation by Ginger ExtractPhenolic Compounds Exerting Lipid-Regulatory, Anti-Inflammatory and Epigenetic Effects as Complementary Treatments in Cardiovascular DiseasesAssociation of APOA5 and APOC3 gene polymorphisms with plasma apolipoprotein A5 level in patients with metabolic syndrome
P50
Q24294997-EBE1162D-1EA3-45CC-879F-3502069A46B5Q35814698-462C480E-7503-486F-80E6-15995877CBDCQ36102976-C7D305EE-1D37-47D8-BD4E-8A29D0CE3138Q38780771-137AC49B-4A82-4B68-928C-B4C48F17A0DCQ39174195-9B0D7974-7314-4492-82E3-340F8BDE21E8Q41260650-AD8E53BA-62ED-4132-975C-0D32833D540CQ42009667-B9F817AB-4849-4EA1-8B18-2834738CB3C8Q44662236-D262D285-89E1-4F54-96B3-FAFD39CF898BQ46792665-B81068A9-D1D3-4168-8007-2C950E52BE88Q51741393-3BDD6E2E-6863-4D2B-8A17-AEECD29C033BQ88564301-1EAADAFA-7D53-42F4-B171-72B6E5D63DFEQ91797779-5F36CD49-6B95-4B46-9D3E-097963BCD242Q93188805-C46950DE-9BF5-416F-9952-D4172FDD875CQ94947648-0B1BB74B-02EA-4250-88C5-C40FECA70C89
P50
description
onderzoeker
@nl
researcher
@en
հետազոտող
@hy
name
Loredan S Niculescu
@nl
Loredan S Niculescu
@sl
Loredan S. Niculescu
@en
Loredan S. Niculescu
@es
type
label
Loredan S Niculescu
@nl
Loredan S Niculescu
@sl
Loredan S. Niculescu
@en
Loredan S. Niculescu
@es
prefLabel
Loredan S Niculescu
@nl
Loredan S Niculescu
@sl
Loredan S. Niculescu
@en
Loredan S. Niculescu
@es
P1053
F-2591-2010
P106
P1153
6603212488
P31
P3829
P496
0000-0002-1394-9085