(1) Background: Ferroptosis is a newly coined form of programmed cell death marked by lethal accumulation of lipid peroxidation and ferrous iron overload. A few studies on the specific mechanism of ferroptosis in the genesis and development of psoriasis are available. (2) Methods: Levels of lipid reactive oxygen species (ROS) and ferrous iron were measured by flow cytometry. Ultrastructure analysis was performed by transmission electron microscopy. Imiquimod-induced psoriasis-like mice were treated with a ferroptosis inducer. The expressions of mRNA of genes were measured by qRT-PCR. HaCaT cells were used to explore the function of Cyb561d2. (3) Results: In this work, we observed that levels of lipid ROS and ferrous iron in the epidermis of psoriasis vulgaris (PV) patients were increased. The existence of ferroptosis activation in the epidermis of individuals with PV was confirmed by transmission electron microscope both in patients with PV and psoriasis-like mice models. Intradermal injection of the ferroptosis inducer RSL3 in psoriasis-like mice significantly promoted and aggravated the development of psoriasis-like dermatitis, and the level of serum transferrin was also increased in PV samples. Moreover, abnormal expression of some genes related to iron metabolism was also proved in the epidermis of PV cases, among which Cyb561d2 was shown to promote ferrous iron overload and lipid peroxidation accumulation in HaCaT cells. (4) Conclusions: In summary, our study suggested that ferroptosis activation owing to iron overload may be a novel mechanism underlying the formation of skin lesions in individuals with PV.

中文翻译：

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Ferroptosis 激活有助于寻常型银屑病皮肤损伤的形成。

(1) 背景：Ferroptosis 是一种新创造的程序性细胞死亡形式，其特征是脂质过氧化作用的致死积累和亚铁过载。铁死亡在银屑病发生发展过程中的具体机制研究较少。(2)方法：采用流式细胞术检测脂质活性氧(ROS)和亚铁水平。通过透射电子显微镜进行超微结构分析。用铁死亡诱导剂治疗咪喹莫特诱导的银屑病样小鼠。通过qRT-PCR测量基因mRNA的表达。HaCaT 细胞用于探索 Cyb561d2 的功能。(3) 结果：在这项工作中，我们观察到寻常型银屑病 (PV) 患者表皮中脂质 ROS 和二价铁的水平升高。在 PV 患者和银屑病样小鼠模型中，通过透射电子显微镜证实了 PV 个体表皮中铁死亡激活的存在。银屑病样小鼠皮内注射铁死亡诱导剂RSL3显着促进和加重银屑病样皮炎的发展，PV样本中血清转铁蛋白水平也升高。此外，在PV病例的表皮中也证实了一些与铁代谢相关的基因异常表达，其中Cyb561d2显示出促进HaCaT细胞中亚铁过载和脂质过氧化积累。(4) 结论：总之，我们的研究表明，铁过载导致的铁死亡激活可能是 PV 患者皮肤损伤形成的一种新机制。