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Fibrosis and Adipose Tissue Dysfunction

Journal

CELL METABOLISM
Volume 18, Issue 4, Pages 470-477

Publisher

CELL PRESS
DOI: 10.1016/j.cmet.2013.06.016

Keywords

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Funding

  1. National Institutes of Health [R01-DK55758, R01-DK099110, P01DK088761]
  2. Juvenile Diabetes Research Foundation [JDRF 17-2012-36]
  3. French National Agency of Research (ANR-Adipofib)
  4. Fondation pour la Recherche Medicale (FRM)
  5. Assistance Publique Hopitaux de Paris, APHP (Clinical Research Contract, CRC fibrota)

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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 alpha 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.

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