期刊
CURRENT OPINION IN CLINICAL NUTRITION AND METABOLIC CARE
卷 12, 期 4, 页码 404-411出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MCO.0b013e32832c7819
关键词
adiponectin; endocannabinoids; innate immunity; leptin; renin-angiotensin system
资金
- Belgian National Funds for Scientific Research [3.4578.07]
- la Direction de la Recherche Scientifique de la Communaute Franraise de Belgique [05/10-328]
- University FSR
Purpose of review To highlight the metabolic or inflammatory components, deregulated in or pathogenic for the metabolic syndrome, that may, directly or indirectly, modulate hepatic fibrogenesis. Recent findings Advanced glycation end products signal profibrogenetic transformation of hepatic stellate cells. Altered adipocytokines favor insulin resistance and steatosis. They participate to the proinflammatory status of the metabolic syndrome. Among them, leptin has been shown to directly enhance fibrogenesis, whereas adiponectin has shown antifibrotic properties. The renin-angiotensin system, a component of arterial hypertension, is activated in the diseased liver, and there is convincing evidence that blockade of angiotensin 11 signaling attenuates fibrosis. Endocannabinoids, whose hepatic production and signaling capability are increased with insulin resistance and obesity, signal profibrotic response via the preponderant receptor, cannabinoid receptor 1, whereas antifibrotic and anti-inflammatory signals are rather generated via stimulation of cannabinoid receptor 2. Finally, recent data demonstrate that modulation of innate immunity, particularly modulation of natural killer and natural killer T cells, has potential roles in the resolution of steatohepatitis and fibrosis. Summary Several features associated with the metabolic syndrome can undoubtedly modulate liver fibrosis. More studies are needed to identify those that are prominent determinants of fibrosis in the metabolic syndrome and the benefit of their targeting for fibrosis prevention and treatment.
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