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摘要:
Psoriasis has been lately seen as a potential systemic inflammatory disease associated with a range of comorbidities exhibiting an overlapping pathology and presenting a great social health impact such as cardiovascular disease and metabolic diseases,including obesity.Adipose tissue is considered a genuine endocrine organ producing a variety of bioactive adipocytokines,like leptin,adiponectin,resistin and visfatin,participating in physiological and pathological processes,such as energy balance,insulin sensitivity and resistance,immunity,inflammation,hematopoiesis and angiogenesis.Adipocytokines could serve as a missing link in the association between psoriasis,obesity and metabolic co-morbidities.In chronic inflammatory disease states such as psoriasis,adipocytokines may be implicated in psoriasis onset,progression,severity as well as in the pathogenesis of co-morbidities.Measuring serum adipocytokine levels in the future may be useful in predicting psoriasis severity,progression,treatment outcome and risk of any co-morbidities.Interventions to decrease pro-inflammatory adipocytokine levels could offer preventive and therapeutic options for improving psoriasis severity and protecting against its co-morbidities.Candidate strategic interventions incorporate increased physical activity,weight control and pharmacologic approaches such as metformin.However,the mechanisms underlying the actions of adipocytokines in psoriasis as well as their potential diagnostic,prognostic and/or therapeutic utility require further investigation with larger prospective,longitudinal and mechanistic studies.
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篇名 Adipocytokines and psoriasis:Insights into mechanisms linking obesity and inflammation to psoriasis
来源期刊 世界皮肤病学杂志 学科 医学
关键词 PSORIASIS ADIPOCYTOKINE OBESITY Leptin ADIPONECTIN Omentin RESISTIN Visfatin
年,卷(期) 2013,(4) 所属期刊栏目
研究方向 页码范围 27-31
页数 5页 分类号 R
字数 语种
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研究主题发展历程
节点文献
PSORIASIS
ADIPOCYTOKINE
OBESITY
Leptin
ADIPONECTIN
Omentin
RESISTIN
Visfatin
研究起点
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研究分支
研究去脉
引文网络交叉学科
相关学者/机构
期刊影响力
世界皮肤病学杂志
不定期
2218-6190
北京市朝阳区东四环中路62号楼远洋国际中
出版文献量(篇)
72
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0
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0
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