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Jean-Charles Fruchart

Researcher at Lille University of Science and Technology

Publications -  124
Citations -  11956

Jean-Charles Fruchart is an academic researcher from Lille University of Science and Technology. The author has contributed to research in topics: Peroxisome proliferator-activated receptor & Nuclear receptor. The author has an hindex of 53, co-authored 124 publications receiving 11459 citations. Previous affiliations of Jean-Charles Fruchart include university of lille & Pasteur Institute of Lille.

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Activation of proliferator-activated receptors alpha and gamma induces apoptosis of human monocyte-derived macrophages.

TL;DR: It is shown that the PPARα and PPARγ forms are expressed in differentiated human monocyte-derived macrophages, which participate in inflammation control and atherosclerotic plaque formation and demonstrate a novel function of PPAR in human macrophage with likely consequences in inflammation and Atherosclerosis.
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Peroxisome proliferator-activated receptors (PPARs): nuclear receptors at the crossroads between lipid metabolism and inflammation.

TL;DR: Findings indicate a modulatory role for PPARs in the control of the inflammatory response with potential therapeutic applications in inflammation-related diseases, such as atherosclerosis and inflammatory bowel disease.
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CLA-1/SR-BI Is Expressed in Atherosclerotic Lesion Macrophages and Regulated by Activators of Peroxisome Proliferator-Activated Receptors

TL;DR: The data demonstrate that CLA-1/SR-BI is expressed in atherosclerotic lesion macrophages and induced by PPAR activation, identifying a potential role for PPARs in cholesterol homeostasis in atheosclerotic lesions of apoE-null mice treated with either PPARgamma or PPARalpha ligands.
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Pleiotropic Actions of Peroxisome Proliferator–Activated Receptors in Lipid Metabolism and Atherosclerosis

TL;DR: Peroxisome proliferator–activated receptors modulate the onset and evolution of metabolic disorders predisposing to atherosclerosis and exert direct antiatherogenic actions at the level of the vascular wall by regulating gene transcription.