mTORC1在痤疮发病和治疗中的作用

B. Melnik
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引用次数: 5

摘要

寻常痤疮是西方工业化国家以高血糖负荷和牛奶消费为特征的一种常见皮肤病。越来越多的证据表明,西方饮食是营养介导的雷帕霉素复合物1 (mTORC1)信号传导机制靶点增强的主要原因,可能过度刺激皮脂腺细胞生长和皮脂腺脂肪生成,导致皮脂腺增生、脂腺分泌过多、痤疮丙酸杆菌过度生长、生物膜形成和炎性滤泡反应。来自转化研究的大量证据表明,所有抗痤疮药物都通过一个共同的机制起作用:抑制毛囊皮脂腺中夸大的mTORC1信号转导。未来的痤疮治疗应结合饮食和药物干预,通过支持天然或合成mTOR抑制剂的旧石器饮食来减弱mTORC1信号。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of mTORC1 in acne pathogenesis and treatment
Acne vulgaris is a common skin disease in industrialized countries with Western diet characterized by high glycemic load and milk consumption. Accumulating evidence underlines the role of Western diet as a major cause of enhanced nutrient-mediated mechanistic target of rapamycin complex 1 (mTORC1) signaling that may over-stimulate sebocyte growth and sebaceous lipogenesis resulting in sebaceous gland hyperplasia, hyperseborrhoea, Propionibacterium acnes overgrowth with biofilm formation and inflammatory follicular reactions. Substantial evidence from translational research suggests that all anti-acne agents operate by a common mechanism: the attenuation of exaggerated mTORC1 signal transduction in the pilosebaceous follicle. Future acne therapy should combine dietary and pharmacological interventions attenuating mTORC1 signaling by a paleolithic-type diet supported with natural or synthetic mTOR inhibitors.
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