Abstract |
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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Authors | Tsuyoshi Kadomatsu, Motoyoshi Endo, Keishi Miyata, Yuichi Oike |
Journal | Trends in endocrinology and metabolism: TEM
(Trends Endocrinol Metab)
Vol. 25
Issue 5
Pg. 245-54
(May 2014)
ISSN: 1879-3061 [Electronic] United States |
PMID | 24746520
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Copyright | Copyright © 2014 Elsevier Ltd. All rights reserved. |
Chemical References |
- ANGPTL2 protein, human
- Angiopoietin-Like Protein 2
- Angiopoietin-like Proteins
- Angiopoietins
- Integrins
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Topics |
- Angiopoietin-Like Protein 2
- Angiopoietin-like Proteins
- Angiopoietins
(metabolism)
- Animals
- Atherosclerosis
(metabolism)
- Humans
- Inflammation
(metabolism)
- Integrins
(metabolism)
- Neovascularization, Pathologic
(metabolism)
- Signal Transduction
(physiology)
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