Forecasting Fat Fibrosis

Brett Shook; Matthew S Rodeheffer

doi:10.1016/j.cmet.2017.02.019

Forecasting Fat Fibrosis

Cell Metab. 2017 Mar 7;25(3):493-494. doi: 10.1016/j.cmet.2017.02.019.

Authors

Brett Shook¹, Matthew S Rodeheffer²

Affiliations

¹ Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, CT 06520, USA.
² Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, CT 06520, USA; Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06520, USA; Yale Stem Cell Center, Yale University School of Medicine, New Haven, CT 06520, USA. Electronic address: matthew.rodeheffer@yale.edu.

PMID: 28273471
DOI: 10.1016/j.cmet.2017.02.019

Abstract

Excess ECM and fibrosis of white adipose tissue (WAT) is associated with tissue dysfunction and type 2 diabetes. In this issue of Cell Metabolism, Marcelin et al. (2017) elucidate a key mechanism behind WAT fibrosis in which the activation of PDGFRα on adipocyte precursors drives this population toward a fibrotic phenotype.

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MeSH terms

Adipocytes / cytology
Adipose Tissue, White / cytology*
Diabetes Mellitus, Type 2*
Fibrosis
Humans
Phenotype