Molecular Mechanisms and Management of a Cutaneous Inflammatory Disorder: Psoriasis

被引:101
作者
Woo, Yu Ri [1 ]
Cho, Dae Ho [2 ]
Park, Hyun Jeong [1 ]
机构
[1] Catholic Univ Korea, Coll Med, Yeouido St Marys Hosp, Dept Dermatol, Seoul 07345, South Korea
[2] Sookmyung Womens Univ, Dept Life Sci, Seoul 04310, South Korea
基金
新加坡国家研究基金会;
关键词
biologics; epigenetics; genetics; interleukin-23; psoriasis; signaling pathway; small molecules; T helper 17 cells; GENOME-WIDE ASSOCIATION; NF-KAPPA-B; KERATINOCYTE GROWTH-FACTOR; NECROSIS-FACTOR-ALPHA; REGULATORY T-CELLS; SUSCEPTIBILITY LOCUS; EPIDERMAL HYPERPLASIA; ATOPIC-DERMATITIS; PROINFLAMMATORY CYTOKINES; TRANSCRIPTION FACTOR;
D O I
10.3390/ijms18122684
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Psoriasis is a complex chronic inflammatory cutaneous disorder. To date, robust molecular mechanisms of psoriasis have been reported. Among diverse aberrant immunopathogenetic mechanisms, the current model emphasizes the role of Th1 and the IL-23/Th17 axis, skin-resident immune cells and major signal transduction pathways involved in psoriasis. The multiple genetic risk loci for psoriasis have been rapidly revealed with the advent of a novel technology. Moreover, identifying epigenetic modifications could bridge the gap between genetic and environmental risk factors in psoriasis. This review will provide a better understanding of the pathogenesis of psoriasis by unraveling the complicated interplay among immunological abnormalities, genetic risk foci, epigenetic modification and environmental factors of psoriasis. With advances in molecular biology, diverse new targets are under investigation to manage psoriasis. The recent advances in treatment modalities for psoriasis based on targeted molecules are also discussed.
引用
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页数:26
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