Crewe Clair, An Yu Aaron, Scherer Philipp E
J Clin Invest. 2017 Jan 3;127(1):74-82. doi: 10.1172/JCI88883.
There are three dominant contributors to the pathogenesis of dysfunctional adipose tissue (AT) in obesity: unresolved inflammation, inappropriate extracellular matrix (ECM) remodeling and insufficient angiogenic potential. The interactions of these processes during AT expansion reflect both a linear progression as well as feed-forward mechanisms. For example, both inflammation and inadequate angiogenic remodeling can drive fibrosis, which can in turn promote migration of immune cells into adipose depots and impede further angiogenesis. Therefore, the relationship between the members of this triad is complex but important for our understanding of the pathogenesis of obesity. Here we untangle some of these intricacies to highlight the contributions of inflammation, angiogenesis, and the ECM to both "healthy" and "unhealthy" AT expansion.
肥胖状态下功能失调的脂肪组织（AT）发病机制主要有三个关键因素：炎症持续不消、细胞外基质（ECM）重塑不当以及血管生成潜力不足。在脂肪组织扩张过程中，这些过程之间的相互作用既反映了线性进展，也体现了前馈机制。例如，炎症和血管生成重塑不足均可引发纤维化，进而促进免疫细胞迁移至脂肪库，并阻碍进一步的血管生成。因此，这三者之间的关系错综复杂，但对于我们理解肥胖症的发病机制至关重要。在此，我们梳理其中一些复杂关系，以突出炎症、血管生成和细胞外基质对“健康”和“不健康”脂肪组织扩张的影响。
