Touchstone Diabetes Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.
Cell Metab. 2013 Oct 1;18(4):470-7. doi: 10.1016/j.cmet.2013.06.016. Epub 2013 Aug 15.
Fibrosis is increasingly appreciated as a major player in adipose tissue dysfunction. In rapidly expanding adipose tissue, pervasive hypoxia leads to an induction of HIF1α 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.
纤维化越来越被认为是脂肪组织功能障碍的主要参与者。在迅速扩张的脂肪组织中,弥漫性缺氧导致 HIF1α 的诱导,进而导致强有力的促纤维化转录程序。脂肪组织纤维化的病理生理影响可能与纤维化条件在肝脏、心脏和肾脏中一样,在全身代谢改变中发挥同样重要的作用。在这里,我们讨论了我们对啮齿动物和人类脂肪组织中细胞外基质(ECM)过度积累的发生、调节和系统影响的理解的最新进展,以及随之对代谢功能障碍的影响。