Joëlle Magné

ORCID: 0000-0003-0316-4046
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About
Contact & Profiles
Research Areas
  • Atherosclerosis and Cardiovascular Diseases
  • Adipokines, Inflammation, and Metabolic Diseases
  • Autophagy in Disease and Therapy
  • Nitric Oxide and Endothelin Effects
  • Lipid metabolism and biosynthesis
  • Fatty Acid Research and Health
  • Cancer, Lipids, and Metabolism
  • Folate and B Vitamins Research
  • Phagocytosis and Immune Regulation
  • Lipid metabolism and disorders
  • Diet, Metabolism, and Disease
  • Ferroptosis and cancer prognosis
  • Caveolin-1 and cellular processes
  • Cholesterol and Lipid Metabolism
  • Inflammasome and immune disorders
  • Galectins and Cancer Biology
  • MicroRNA in disease regulation
  • Cardiovascular Issues in Pregnancy
  • Eicosanoids and Hypertension Pharmacology
  • Diabetes, Cardiovascular Risks, and Lipoproteins
  • Cell death mechanisms and regulation
  • Congenital heart defects research
  • Renin-Angiotensin System Studies
  • Sesame and Sesamin Research
  • Microbial Metabolic Engineering and Bioproduction

St. Jude Children's Research Hospital
2017-2025

Université Paris Cité
2025

Inserm
2025

Karolinska Institutet
2011-2020

Karolinska University Hospital
2013-2019

Science for Life Laboratory
2016

Leiden University Medical Center
2016

British Heart Foundation
2016

Physiologie de la Nutrition et du Comportement Alimentaire
2008-2009

AgroParisTech
2008-2009

Key augmented processes in atherosclerosis have been identified, whereas less is known about downregulated pathways. Here, we applied a systems biology approach to examine suppressed molecular signatures, with the hypothesis that they may provide insight into mechanisms contributing plaque stability.Muscle contraction, muscle development, and actin cytoskeleton were most pathways (false discovery rate=6.99e-21, 1.66e-6, 2.54e-10, respectively) microarrays from human carotid plaques (n=177)...

10.1161/atvbaha.116.307893 article EN Arteriosclerosis Thrombosis and Vascular Biology 2016-07-29

Abstract. Coca-Prieto I, Kroupa O, Gonzalez-Santos P, Magne J, Olivecrona G, Ehrenborg E, Valdivielso P (Hospital Virgen de la Victoria, Malaga University, Malaga, Spain; Umea Umea; and Karolinska Institutet, Stockholm; Sweden). Childhood-onset chylomicronaemia with reduced plasma lipoprotein lipase activity mass: identification of a novel GPIHBP1 mutation. J Intern Med 2011; 270: 224–228. Objectives. Deficiency in the catabolism triglyceride-rich lipoproteins is main cause childhood-onset...

10.1111/j.1365-2796.2011.02361.x article EN Journal of Internal Medicine 2011-02-18

Perilipin 2 (PLIN2) is the most abundant lipid droplet (LD)-associated protein in nonadipose tissue, and its expression correlates with intracellular accumulation. Here we identified a missense polymorphism, Ser251Pro, that has major effect on structure function, along an influence human plasma triglyceride concentration. The evolutionarily conserved Ser251Pro polymorphism was ClustalW program. Structure modeling using 3D-JigSaw Chimera package revealed Pro251 allele disrupts predicted...

10.1096/fj.13-228759 article EN The FASEB Journal 2013-04-19

Abstract Individuals with a bicuspid aortic valve (BAV) are at significantly higher risk of developing complications than individuals tricuspid valves (TAV) and defective signaling during the embryonic development and/or life time exposure to abnormal hemodynamic have been proposed as underlying factors. However, an explanation for molecular mechanisms aortopathy in BAV has not yet provided. We combined proteomics, RNA analyses, immunohistochemistry, electron microscopy identify differences...

10.1038/srep35712 article EN cc-by Scientific Reports 2016-10-25

Autophagy has emerged as a cell survival mechanism critical for cellular homeostasis, which may play protective role in atherosclerosis. ATG16L1, protein essential early stages of autophagy, been implicated the pathogenesis Crohn's disease. However, it is unknown whether ATG16L1 involved Our aim was to analyze expression carotid atherosclerotic plaques relation markers plaque vulnerability.Histological analysis 143 endarterectomized human revealed that expressed areas surrounding necrotic...

10.1161/atvbaha.114.304840 article EN Arteriosclerosis Thrombosis and Vascular Biology 2015-03-13

Expression of BCL-B, an anti-apoptotic BCL-2 family member, is correlated with worse survival in lung adenocarcinomas. Here, we show that BCL-B can mitigate cell death initiation through interaction the effector protein BOK. We found this promote sublethal mitochondrial outer membrane permeabilization (MOMP) and consequently generate apoptosis-flatliners, which represent a source drug-tolerant persister cells (DTPs). The engagement endothelial-mesenchymal-transition (EMT) further promotes...

10.3390/cells14040246 article EN cc-by Cells 2025-02-09

Hyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis the underlying cause of both myocardial infarction stroke. We have previously shown that Pro251 variant perilipin-2 reduces plasma triglycerides may therefore be beneficial to reduce development.We sought delineate putative effects perlipin-2 on subclinical mechanism by which it acts.A pan-European cohort high-risk individuals where carotid intima-media thickness has been assessed was adopted. Human...

10.1111/joim.12951 article EN cc-by Journal of Internal Medicine 2019-06-28

In contrast to the quality of carbohydrates and lipids, little is known on influence type dietary protein development metabolic or insulin resistance syndrome. Cysteine intake has been recently documented impact sensitivity. The aim this study was determine whether rapeseed protein, an emergent cysteine-rich could inhibit onset For 9 weeks, rats were fed a diet rich in saturated fats sucrose, which also included 20 % either as milk ('Induction' I) (diet R). A third, control group received...

10.1017/s000711450896092x article EN British Journal Of Nutrition 2008-04-08

In Humans, high-fat or high sucrose meals induce transient vascular endothelial dysfunction, which is the hallmark of early atherogenesis. However, little still known regarding how postprandial metabolic challenge by nutrients translates into risk. An animal model to monitor function under different conditions would be useful. ten conscious Wistar Kyoto rats, we have developed a hemodynamic test function, based on rapid, transient, dose-dependent blood pressure decrease after iv...

10.1096/fasebj.21.5.a375-b article EN The FASEB Journal 2007-04-01

High saturated fat/ high sucrose meals induce oxidative stress associated with vascular endothelial dysfunction, an early hallmark in atherogenesis, but the impact of meal protein on homeostasis remains misunderstood. Here, we investigated potential rapeseed protein, emergent cysteine‐rich to modulate adverse effects a high‐fat (HFM). In cross‐over design, 12 healthy rats received 3 isoenergetic HFM (saturated fat: 60%; sucrose: 20%; proteins: 20% total energy) source being either milk (C),...

10.1096/fasebj.22.1_supplement.312.4 article EN The FASEB Journal 2008-03-01

Abstract Background Hyperlipidemia is a major risk factor for cardiovascular disease and atherosclerosis the underlying cause of both myocardial infarction stroke. We have previously shown that Pro251 variant perilipin-2 reduces plasma triglycerides may therefore be beneficial development. Purpose sought to delineate putative effects perlipin-2 on subclinical mechanism by which it acts. Methods A pan-European cohort high-risk individuals where carotid intima-media thickness has been assessed...

10.1093/eurheartj/ehz747.0332 article EN European Heart Journal 2019-10-01

Objective: Autophagy has emerged as a cell survival mechanism critical for cellular homeostasis, which may play protective role in atherosclerosis. ATG16L1, protein essential early stages of autophagy, been implicated the pathogenesis inflammatory diseases such Crohn’s disease. However, it is unknown whether ATG16L1 involved Our aim was to analyze expression carotid atherosclerotic plaques relation markers plaque vulnerability. Approach and results: Histological analysis 143...

10.1161/atvb.35.suppl_1.567 article EN Arteriosclerosis Thrombosis and Vascular Biology 2015-05-01
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