2018
DOI: 10.3390/ijms19041212
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Abstract: Demyelination in multiple sclerosis (MS) cells is the site of several energy metabolic abnormalities driven by dysregulation between the opposed interplay of peroxisome proliferator-activated receptor γ (PPARγ) and WNT/β-catenin pathways. We focus our review on the opposing interactions observed in demyelinating processes in MS between the canonical WNT/β-catenin pathway and PPARγ and their reprogramming energy metabolism implications. Demyelination in MS is associated with chronic inflammation, which is itsel… Show more

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Cited by 42 publications
(38 citation statements)
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References 265 publications
(304 reference statements)
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“…Semple reviewed the function of PPARγ and its variants in metabolic syndrome . In addition, Jia, Chigurupati and Vallée analysed therapeutic potential of PPARγ agonists in diabetes. PPARγ agonists improve insulin sensitivity and treat complications of diabetes.…”
Section: Function and Cellular Roles Of Pparγmentioning
confidence: 99%
“…Semple reviewed the function of PPARγ and its variants in metabolic syndrome . In addition, Jia, Chigurupati and Vallée analysed therapeutic potential of PPARγ agonists in diabetes. PPARγ agonists improve insulin sensitivity and treat complications of diabetes.…”
Section: Function and Cellular Roles Of Pparγmentioning
confidence: 99%
“…Among the endogenous cell processes capable of promoting mitochondrial functions and the endogenous defense mechanisms there are those triggered by the peroxisome proliferator-activated receptor gamma (PPAR-γ) and by the transcription factor nuclear factor-erythroid 2 (NF-E2)-related factor (NRF2) [ 10 , 11 ].…”
Section: Introductionmentioning
confidence: 99%
“…An intriguing example of the interactions between circadian disorders and MS comes from work on the interplay between the PPARγ and the WNT/β-Catenin signalling pathways [138]. PPARγ is a circadian transcription factor [139], know to regulate rhythmic metabolism, including glucose and lipid metabolism, and to have an anti-inflammatory effect by acting on the levels of NF-κB.…”
Section: Multiple Sclerosis (Ms)mentioning
confidence: 99%
“…Impaired OPC differentiation and failure to remyelinate in MS and EAE are, at least in part, a consequence of overactivation of the WNT/β-Catenin signalling pathway. PPARγ absence aggravates EAE pathophysiology, whilst, its agonists have shown anti-inflammatory and neuroprotective effects, in addition to rendering the environment permissive to remyelination and ameliorating both EAE and MS symptoms [138]. Hence, PPARγ agonists appear a promising treatment to promote remyelination by abolishing the prohibitive effects of the WNT/beta-catenin pathway through regulation of NF-κB activity.…”
Section: Multiple Sclerosis (Ms)mentioning
confidence: 99%