2015 年 35 巻 4 号 p. 193-202
Repeated cellular stress due to aging and lifestyle-related activities causes tissue damage. That damage is repaired by a homeostatic process consisting first of acute inflammation and then of adaptive physiologic tissue remodeling meditated by communication between parenchymal and stromal cells. That signaling can occur via cell-to-cell contact or through secreted factors. However, excessive or prolonged stress leads to chronic inflammation and pathologic tissue remodeling, perturbing homeostasis and promoting development of lifestyle-related diseases or cancer. Expression of Angiopoietin-like protein 2 (ANGPTL2) is induced both normally and by disease-associated stresses. In the former, ANGPTL2 promotes proper adaptive inflammation and tissue reconstruction and thus maintains homeostasis; however, in the latter, excess ANGPTL2 activation impairs homeostasis due to chronic inflammation and irreversible tissue remodeling, promoting metabolic and atherosclerotic diseases and some cancers. Thus, it is important to define how ANGPTL2 signaling is regulated in order to understand mechanisms underlying tissue homeostasis and disease development. Here, we focus on ANGPTL2 function in these activities and discuss whether excess ANGPTL2 function is a common molecular mechanism underlying lifestyle diseases and cancer.
