Abstract:
:Psoriasis is a common chronic inflammatory multisystemic disease with a complex pathogenesis consisting of genetic, immunological, and environmental components. It is associated with a number of comorbidities, including diabetes, metabolic syndrome, obesity, and myocardial infarction. In addition, the severity of psoriasis seems to be related to the severity of obesity. Patients with higher levels of obesity show poorer response to systemic treatments of psoriasis. Several studies have demonstrated that white adipose tissue is a crucial site of the formation of proinflammatory adipokines such as leptin, adiponectin, and resistin and classical cytokines such as interleukin- (IL-) 6 and tumour necrosis factor-α. In psoriasis, due to the proliferation of Th1, Th17, and Th22 cells, IL-22, among others, is produced in addition to the abovementioned cytokines. With respect to leptin and resistin, both of these adipokines are present in high levels in obese persons with psoriasis. Further, the plasma levels of leptin and resistin are related to the severity of psoriasis. These results strongly suggest that obesity, through proinflammatory pathways, is a predisposing factor to the development of psoriasis and that obesity aggravates existing psoriasis. Different inflammatory biomarkers link psoriasis and obesity. In this paper, the most important ones are described.
journal_name
Mediators Inflammjournal_title
Mediators of inflammationauthors
Rodríguez-Cerdeira C,Cordeiro-Rodríguez M,Carnero-Gregorio M,López-Barcenas A,Martínez-Herrera E,Fabbrocini G,Sinani A,Arenas-Guzmán R,González-Cespón JLdoi
10.1155/2019/7353420subject
Has Abstractpub_date
2019-05-28 00:00:00pages
7353420eissn
0962-9351issn
1466-1861journal_volume
2019pub_type
杂志文章,评审abstract::Nitrooleic acid (OA-NO2) is an endogenous lipid product which has novel signaling properties, particularly the activation of peroxisome proliferator-activated receptors. The current study aimed to evaluate the protective effects of OA-NO2 against cisplatin-induced kidney injury in mice. Mice were pretreated with OA-NO...
journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
pub_type: 杂志文章,收录出版
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journal_title:Mediators of inflammation
pub_type: 杂志文章,评审
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