Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, CT 06520, USA.
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.
Cell Metab. 2017 Mar 7;25(3):493-494. doi: 10.1016/j.cmet.2017.02.019.
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.
细胞外基质（ECM）过剩和白色脂肪组织（WAT）纤维化与组织功能障碍和 2 型糖尿病有关。在本期《细胞代谢》中，Marcelin 等人阐明了 WAT 纤维化背后的一个关键机制，即脂肪细胞前体细胞上 PDGFRα 的激活促使该细胞群向纤维表型发展。
