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240908s2024 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2024.110357
|2 doi
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|a eng
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|a Masuyama, Satoshi
|e verfasserin
|4 aut
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|a Enhanced fatty acid oxidation by selective activation of PPARα alleviates autoimmunity through metabolic transformation in T-cells
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|c 2024
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
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|2 rdacarrier
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|a Date Completed 04.11.2024
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|a Date Revised 04.11.2024
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.
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|a While fatty acid oxidation (FAO) in mitochondria is a primary energy source for quiescent lymphocytes, the impact of promoting FAO in activated lymphocytes undergoing metabolic reprogramming remains unclear. Here, we demonstrate that pemafibrate, a selective PPARα modulator used clinically for the treatment of hypertriglyceridemia, transforms metabolic system of T-cells and alleviates several autoimmune diseases. Pemafibrate suppresses Th17 cells but not Th1 cells, through the inhibition of glutaminolysis and glycolysis initiated by enhanced FAO. In contrast, a conventional PPARα agonist fenofibrate significantly inhibits cell growth by restraining overall metabolisms even at a dose insufficient to induce fatty acid oxidation. Clinically, patients receiving pemafibrate showed a significant decrease of Th17/Treg ratio in peripheral blood. Our results suggest that augmented FAO by pemafibrate-mediated selective activation of PPARα restrains metabolic programs of Th17 cells and could be a viable option for the treatment of autoimmune diseases
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|a Journal Article
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|a Autoimmunity
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|a FAO
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|a Glutaminolysis
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|a PPARα
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|a Th17
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|a PPAR alpha
|2 NLM
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|a Fatty Acids
|2 NLM
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|a Butyrates
|2 NLM
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| 650 |
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|a Fenofibrate
|2 NLM
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| 650 |
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|a U202363UOS
|2 NLM
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| 650 |
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|a (R)-2-(3-((benzoxazol-2-yl-d4 (3-(4-methoxyphenoxy-d7)propyl)amino)methyl)phenoxy) butanoic acid
|2 NLM
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| 650 |
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|a Benzoxazoles
|2 NLM
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| 700 |
1 |
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|a Mizui, Masayuki
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Morita, Masashi
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Shigeki, Takatomo
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Kato, Hisakazu
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Yamamoto, Takeshi
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Sakaguchi, Yusuke
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Inoue, Kazunori
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Namba-Hamano, Tomoko
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Matsui, Isao
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Okuno, Tatsusada
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Yamamoto, Ryohei
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Takashima, Seiji
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Isaka, Yoshitaka
|e verfasserin
|4 aut
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| 773 |
0 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 268(2024) vom: 01. Nov., Seite 110357
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnas
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| 773 |
1 |
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|g volume:268
|g year:2024
|g day:01
|g month:11
|g pages:110357
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|u http://dx.doi.org/10.1016/j.clim.2024.110357
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