Author(s): Sun K, Tordjman J, Clment K, Scherer PE
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Abstract Fibrosis is increasingly appreciated as a major player in adipose tissue dysfunction. In rapidly expanding adipose tissue, pervasive hypoxia leads to an induction of HIF1╬▒ that in turn leads to a potent profibrotic transcriptional program. The pathophysiological impact of adipose tissue fibrosis is likely to play an equally important role on systemic metabolic alterations as fibrotic conditions play in the liver, heart, and kidney. Here, we discuss recent advances in our understanding of the genesis, modulation, and systemic impact of excessive extracellular matrix (ECM) accumulation in adipose tissue of both rodents and humans and the ensuing impact on metabolic dysfunction. Copyright ┬ę 2013 Elsevier Inc. All rights reserved.
This article was published in Cell Metab
and referenced in Journal of Clinical & Cellular Immunology