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Diabetes Mellitus Is Associated With Reduced High-Density Lipoprotein Sphingosine-1-Phosphate Content and Impaired High-Density Lipoprotein Cardiac Cell Protection

Publié dansArteriosclerosis, Thrombosis, and Vascular Biology, vol. 36, no. 5, p. 817-824
Date de publication2016
Résumé

The dyslipidemia of type 2 diabetes mellitus has multiple etiologies and impairs lipoprotein functionality, thereby increasing risk for cardiovascular disease. High-density lipoproteins (HDLs) have several beneficial effects, notably protecting the heart from myocardial ischemia. We hypothesized that glycation of HDL could compromise this cardioprotective effect.

Mots-clés
  • Animals
  • Animals, Newborn
  • Case-Control Studies
  • Cell Survival
  • Cells, Cultured
  • Diabetes Mellitus, Type 2/blood/complications/diagnosis
  • Diabetic Cardiomyopathies/blood/diagnosis/etiology/prevention & control
  • Dyslipidemias/blood/diagnosis/etiology
  • Genotype
  • Glycosylation
  • Hemoglobin A, Glycosylated/metabolism
  • Humans
  • Isolated Heart Preparation
  • Lipoproteins, HDL/blood
  • Lysophospholipids/blood
  • Male
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Myocardial Reperfusion Injury/metabolism/pathology/prevention & control
  • Myocytes, Cardiac/metabolism/pathology
  • Oxidative Stress
  • Phenotype
  • RNA Interference
  • Rats, Wistar
  • Scavenger Receptors, Class B/deficiency/genetics/metabolism
  • Sphingosine/analogs & derivatives/blood
  • Time Factors
  • Transfection
Citation (format ISO)
BRINCK, Jonas et al. Diabetes Mellitus Is Associated With Reduced High-Density Lipoprotein Sphingosine-1-Phosphate Content and Impaired High-Density Lipoprotein Cardiac Cell Protection. In: Arteriosclerosis, Thrombosis, and Vascular Biology, 2016, vol. 36, n° 5, p. 817–824. doi: 10.1161/ATVBAHA.115.307049
Fichiers principaux (1)
Article (Published version)
accessLevelRestricted
Identifiants
ISSN du journal1079-5642
494vues
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Informations techniques

Création13/09/2017 13:53:00
Première validation13/09/2017 13:53:00
Heure de mise à jour15/03/2023 02:02:38
Changement de statut15/03/2023 02:02:37
Dernière indexation02/05/2024 19:30:49
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