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Redox mechanisms in regulation of adipocyte differentiation: beyond a general stress response


Liu, GS and Chan, EC and Higuchi, M and Dusting, GJ and Jiang, F, Redox mechanisms in regulation of adipocyte differentiation: beyond a general stress response, Cells, 1, (4) pp. 976-993. ISSN 2073-4409 (2012) [Refereed Article]


Copyright Statement

2012 by the authors. Licensed under Creative Commons Attribution 3.0 Unported (CC BY 3.0)

DOI: doi:10.3390/cells1040976


In this review, we summarize advances in our understanding of redox-sensitive mechanisms that regulate adipogenesis. Current evidence indicates that reactive oxygen species may act to promote both the initiation of adipocyte lineage commitment of precursor or stem cells, and the terminal differentiation of preadipocytes to mature adipose cells. These can involve redox regulation of pathways mediated by receptor tyrosine kinases, peroxisome proliferator-activated receptor γ (PPARγ), PPARγ coactivator 1α (PGC-1α), AMP-activated protein kinase (AMPK), and CCAAT/enhancer binding protein β (C/EBPβ). However, the precise roles of ROS in adipogenesis in vivo remain controversial. More studies are needed to delineate the roles of reactive oxygen species and redox signaling mechanisms, which could be either positive or negative, in the pathogenesis of obesity and related metabolic disorders.

Item Details

Item Type:Refereed Article
Keywords:adipocyte, adipogenesis, differentiation, obesity, oxidative stress, reactive oxygen species, redox regulation
Research Division:Biomedical and Clinical Sciences
Research Group:Medical biotechnology
Research Field:Gene and molecular therapy
Objective Division:Health
Objective Group:Clinical health
Objective Field:Clinical health not elsewhere classified
UTAS Author:Liu, GS (Associate Professor Guei-Sheung Liu)
ID Code:120863
Year Published:2012
Deposited By:Menzies Institute for Medical Research
Deposited On:2017-08-31
Last Modified:2017-09-08
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