Retinoids Issued from Hepatic Stellate Cell Lipid Droplet Loss as Potential Signaling Molecules Orchestrating a Multicellular Liver Injury Response

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Retinoids Issued from Hepatic Stellate Cell Lipid Droplet Loss as Potential Signaling Molecules Orchestrating a Multicellular Liver Injury Response

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scientific article published on 13 September 2018

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wetenschappelijk artikel

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наукова стаття, опублікована у вересні 2018

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Retinoids Issued from Hepatic ...... cellular Liver Injury Response

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Retinoids Issued from Hepatic ...... cellular Liver Injury Response

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Retinoids Issued from Hepatic ...... cellular Liver Injury Response

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Retinoids Issued from Hepatic ...... cellular Liver Injury Response

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Retinoids Issued from Hepatic ...... cellular Liver Injury Response

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Retinoids Issued from Hepatic ...... cellular Liver Injury Response

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P1476

Retinoids Issued from Hepatic ...... cellular Liver Injury Response

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Philippe Lefebvre

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Retinoid absorption and storage is impaired in mice lacking lecithin:retinol acyltransferase (LRAT).

Replacement of retinyl esters by polyunsaturated triacylglycerol species in lipid droplets of hepatic stellate cells during activation

Biological functional annotation of retinoic acid alpha and beta in mouse liver based on genome-wide binding.

Hepatocyte-specific mutation establishes retinoid X receptor alpha as a heterodimeric integrator of multiple physiological processes in the liver.

Distinct populations of hepatic stellate cells in the mouse liver have different capacities for retinoid and lipid storage.

Hepatic stellate cell lipid droplets: a specialized lipid droplet for retinoid storage.

Selective ablation of retinoid X receptor alpha in hepatocytes impairs their lifespan and regenerative capacity.

Genome-wide profiling of liver X receptor, retinoid X receptor, and peroxisome proliferator-activated receptor α in mouse liver reveals extensive sharing of binding sites

Microbiota and bile acid profiles in retinoic acid-primed mice that exhibit accelerated liver regeneration.

Myofibroblasts revert to an inactive phenotype during regression of liver fibrosis

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137

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scholarly article

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10.3390/CELLS7090137

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English

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Bart Staels

Jerome Eeckhoute

Francesco Paolo Zummo

Marie Bobowski-Gérard

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2018-09-13T00:00:00Z

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30217095

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6162435

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