炎症
平衡
组织重塑
病理生理学
病态的
间质细胞
细胞生物学
生物
医学
病理
免疫学
作者
Tsuyoshi Kadomatsu,Motoyoshi Endo,Keishi Miyata,Yuichi Oike
标识
DOI:10.1016/j.tem.2014.03.012
摘要
Stresses based on aging and lifestyle can cause tissue damage. Repair of damage by tissue remodeling is often meditated by communications between parenchymal and stromal cells via cell-cell contact or humoral factors. However, loss of tissue homeostasis leads to chronic inflammation and pathological tissue remodeling. Angiopoietin-like protein 2 (ANGPTL2) maintains tissue homeostasis by promoting adaptive inflammation and subsequent tissue reconstruction, whereas excess ANGPTL2 activation induced by prolonged stress promotes breakdown of tissue homeostasis due to chronic inflammation and irreversible tissue remodeling, promoting development of various metabolic diseases. Thus, it is important to define how ANGPTL2 signaling is regulated in order to understand mechanisms underlying disease development. Here, we focus on ANGPTL2 function in physiology and pathophysiology.
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