Abstract：
Autophagy is a lysosome-dependent, self-renewal mechanism that degrades and recycles cellular components in eukaryotic cells to maintain the homeostasis of the intracellular environment. Psoriasis is featured by increased inflammatory response, epidermal hyperproliferation and abnormal differentiation, infiltration of immune cells and increased expression levels of both endothelial adhesion molecules and angiogenic mediators. Evidence indicates that autophagy has important roles in many different types of cells, such as lymphocytes, keratinocytes, monocytes and mesenchymal stem cells (MSCs). This paper will review the role of autophagy in the pathogenesis of psoriasis and strategies for therapeutic modulation. Key Message Autophagy regulates the functions of cutaneous cells (MSCs, KCs, T cells and endothelial cells). Since reduced autophagy contributes in part to the pathogenesis of psoriasis, enhancement of autophagy can be an alternative approach to mitigate psoriasis.
摘要：
自噬是一种溶酶体依赖性,自我更新机制，它降解和再循环真核细胞中的细胞成分以维持细胞内环境的稳态。牛皮癣的特点是炎症反应增加，表皮过度增殖和异常分化，免疫细胞浸润和内皮粘附分子和血管生成介质的表达水平增加。证据表明，自噬在许多不同类型的细胞中具有重要作用。如淋巴细胞，角质形成细胞，单核细胞和间充质干细胞（MSC）。本文就自噬在银屑病发病机制中的作用及治疗调控策略作一综述。关键信息自噬调节皮肤细胞的功能（MSCs，KC,T细胞和内皮细胞）。由于减少的自噬部分有助于银屑病的发病机制，增强自噬可能是减轻银屑病的另一种方法。
