Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto 860-8556, Japan.
Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto 860-8556, Japan; Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Chiyoda-ku, Tokyo 102-0075, Japan.
Trends Endocrinol Metab. 2014 May;25(5):245-54. doi: 10.1016/j.tem.2014.03.012. Epub 2014 Apr 17.
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.
基于衰老和生活方式的压力会导致组织损伤。组织重塑通过实质细胞和基质细胞之间的细胞-细胞接触或体液因子的通讯来修复损伤。然而，组织内稳态的丧失会导致慢性炎症和病理性组织重塑。血管生成素样蛋白 2（ANGPTL2）通过促进适应性炎症和随后的组织重建来维持组织内稳态，而长期应激引起的过量 ANGPTL2 激活会导致慢性炎症和不可逆的组织重塑引起的组织内稳态破坏，促进各种代谢疾病的发展。因此，重要的是要确定 ANGPTL2 信号如何受到调节，以便了解疾病发展的机制。在这里，我们专注于 ANGPTL2 在生理和病理生理学中的功能。
