BACKGROUND Sebaceous glands (SGs) are appendages of mammalian skin that produce a mixture of lipids known as sebum. Acne vulgaris is an exceptionally common skin condition, characterized by elevated sebum production, altered sebum composition, and the formation of infundibular cysts, called comedones. Comedo-associated SGs are atrophic, suggesting that comedo formation involves abnormal differentiation of progenitor cells that generate the SG and infundibulum: the 'comedo switch'. Understanding the biological processes that govern SG homeostasis promises to highlight potential aetiological mechanisms underlying acne and other SG-associated skin disorders. RESULTS In this review, we discuss the clinical data, genetic mouse models and in vitro research that have highlighted major hormones, paracrine factors, transcription factors and signalling pathways that control SG homeostasis. These include, but are not limited to androgens, progestogens and oestrogens; retinoids; receptor tyrosine kinases such as ErbB family receptors, fibroblast growth factor receptor 2 and insulin/insulin-like growth factor 1 receptors; peroxisome proliferator-activated receptor γ; aryl hydrocarbon receptor; and the Wnt signalling pathway. Where possible, the cellular and molecular mechanisms by which these regulatory factors control SG biology are indicated, along with considerations as to how they might contribute to acne pathogenesis. CONCLUSIONS Future research should seek to establish the relative importance, and causative relationships, of altered sebum production, sebum composition, inflammation and abnormal differentiation of sebaceous progenitors to the process of comedo formation in acne. Such an understanding will allow for therapeutic targeting of regulatory factors that control SG homeostasis, with the aim of treating acne.

中文翻译：

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皮脂腺的稳态和痤疮的发病机理。

背景技术皮脂腺（SGs）是哺乳动物皮肤的附肢，其产生称为皮脂的脂质混合物。寻常痤疮是一种异常常见的皮肤病，其特征是皮脂分泌增加，皮脂成分改变以及形成称为粉刺的漏斗状囊肿。与粉刺相关的SGs是萎缩的，这表明粉刺的形成涉及产生SG和漏斗的祖细胞的异常分化：“粉刺开关”。了解控制SG稳态的生物学过程有望突出痤疮和其他与SG相关的皮肤疾病的潜在病因机制。结果在这篇综述中，我们讨论了突出主要激素，旁分泌因子，控制SG稳态的转录因子和信号通路。这些包括但不限于雄激素，孕激素和雌激素；类维生素A; 受体酪氨酸激酶，例如ErbB家族受体，成纤维细胞生长因子受体2和胰岛素/胰岛素样生长因子1受体；过氧化物酶体增殖物激活受体γ；芳烃受体 和Wnt信号通路。在可能的地方，指出了这些调节因子控制SG生物学的细胞和分子机制，并考虑了它们可能如何促进痤疮的发病机理。结论未来的研究应寻求确定皮脂生产，皮脂成分改变，皮脂祖细胞的炎症和异常分化导致痤疮粉刺形成的过程。这样的理解将允许控制SG稳态的调节因子的治疗靶点，从而治疗痤疮。