GDF15 mediates the metabolic effects of PPARβ/δ by activating AMPK-Reference-Cited by-同舟云学术

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GDF15 mediates the metabolic effects of PPARβ/δ by activating AMPK

Published:2021-08 Issue:6 Volume:36 Page:109501
ISSN:2211-1247
Container-title:Cell Reports
language:en
Short-container-title:Cell Reports

Author:

Aguilar-Recarte David,Barroso Emma,Gumà Anna,Pizarro-Delgado Javier,Peña Lucía,Ruart Maria,Palomer Xavier,Wahli Walter,Vázquez-Carrera Manuel

Publisher

Elsevier BV

Subject

General Biochemistry, Genetics and Molecular Biology

Reference58 articles.

1. GDF15, a cardioprotective TGF-beta superfamily protein;Ago;Circ. Res.,2006

2. GDF-15 inhibits integrin activation and mouse neutrophil recruitment through the ALK-5/TGF-βRII heterodimer;Artz;Blood,2016

3. Expression of NAG-1, a transforming growth factor-beta superfamily member, by troglitazone requires the early growth response gene EGR-1;Baek;J. Biol. Chem.,2004

4. Cyclooxygenase inhibitors induce the expression of the tumor suppressor gene EGR-1, which results in the up-regulation of NAG-1, an antitumorigenic protein;Baek;Mol. Pharmacol.,2005

5. The PPARβ/δ activator GW501516 prevents the down-regulation of AMPK caused by a high-fat diet in liver and amplifies the PGC-1α-Lipin 1-PPARα pathway leading to increased fatty acid oxidation;Barroso;Endocrinology,2011

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5. Overview of growth differentiation factor 15 (GDF15) in metabolic diseases;Biomedicine & Pharmacotherapy;2024-07

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