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Redox Mechanisms in Regulation of Adipocyte Differentiation: Beyond a General Stress Response
Centre for Eye Research Australia, University of Melbourne, Victoria 3002, Australia
Key Laboratory of Cardiovascular Remodeling and Function Research, Qilu Hospital, Shandong University, Jinan 250-012, Shandong, China
* Author to whom correspondence should be addressed.
Received: 28 September 2012; in revised form: 26 October 2012 / Accepted: 31 October 2012 / Published: 5 November 2012
Abstract: 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.
Keywords: adipocyte; adipogenesis; differentiation; obesity; oxidative stress; reactive oxygen species; redox regulation
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Cite This Article
MDPI and ACS Style
Liu, G.-S.; Chan, E.C.; Higuchi, M.; Dusting, G.J.; Jiang, F. Redox Mechanisms in Regulation of Adipocyte Differentiation: Beyond a General Stress Response. Cells 2012, 1, 976-993.
Liu G-S, Chan EC, Higuchi M, Dusting GJ, Jiang F. Redox Mechanisms in Regulation of Adipocyte Differentiation: Beyond a General Stress Response. Cells. 2012; 1(4):976-993.
Liu, Guei-Sheung; Chan, Elsa C.; Higuchi, Masayoshi; Dusting, Gregory J.; Jiang, Fan. 2012. "Redox Mechanisms in Regulation of Adipocyte Differentiation: Beyond a General Stress Response." Cells 1, no. 4: 976-993.