Effect of AMP-activated protein kinase on cardiovascular protection of adiponectin.
- Author:
Li LI
1
;
Li-Ling WU
Author Information
1. Department of Physiology and Pathophysiology, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University Health Science Center, Beijing 100083, China.
- Publication Type:Journal Article
- MeSH:
AMP-Activated Protein Kinases;
metabolism;
Adiponectin;
physiology;
Animals;
Cardiomegaly;
Cardiovascular Diseases;
physiopathology;
Energy Metabolism;
Glucose;
Heart;
Humans;
Multienzyme Complexes;
Phosphorylation;
Protein-Serine-Threonine Kinases
- From:
Acta Physiologica Sinica
2007;59(5):614-618
- CountryChina
- Language:Chinese
-
Abstract:
Adiponectin, derived mainly from white adipose tissue, regulates glucose and fatty acid metabolism and has anti-inflammatory and anti-atherosclerotic properties. The decrease in plasma adiponectin concentration contributes to the development of metabolic and cardiovascular diseases. AMP-activated protein kinase (AMPK) is a serine/threonine kinase which plays an important role in regulating many cellular processes, particularly pathways involved in cellular energy status. AMPK is now recognized as a fuel gauge in mammalian cells. Adiponectin activates AMPK phosphorylation and then promotes ATP-generating pathways in heart, including glucose transport, glycolysis, and fatty acid oxidation. The recent evidence has shown that AMPK activation has an important role in the vasculature where it may exert anti-atherosclerotic effects. Phosphorylation of AMPK induced by adiponectin inhibits protein synthesis, and may be an adaptive response to pathological cardiac hypertrophy. AMPK also has a cardioprotective role against myocardial injury and apoptosis in the ischemic heart. This review will discuss the role of AMPK in adiponectin-mediated protective properties of cardiovascular diseases.
