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银屑病患者的蛋白质加合物与脂质过氧化产物。

Protein adducts with lipid peroxidation products in patients with psoriasis.

机构信息

Dermatological Specialized Center "DERMAL" NZOZ in Bialystok, Poland.

Department of Analytical Chemistry, Medical University of Bialystok, Poland.

出版信息

Redox Biol. 2023 Jul;63:102729. doi: 10.1016/j.redox.2023.102729. Epub 2023 May 3.

DOI:10.1016/j.redox.2023.102729
PMID:37150149
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10195986/
Abstract

Psoriasis, one of the most frequent immune-mediated skin diseases, is manifested by numerous psoriatic lessons on the skin caused by excessive proliferation and keratinization of epidermal cells. These disorders of keratinocyte metabolism are caused by a pathological interaction with the cells of the immune system, including lymphocytes, which in psoriasis are also responsible for systemic inflammation. This is accompanied by oxidative stress, which promotes the formation of lipid peroxidation products, including reactive aldehydes and isoprostanes, which are additional pro-inflammatory signaling molecules. Therefore, the presented review is focused on highlighting changes that occur during psoriasis development at the level of lipid peroxidation products, including 4-hydroxynonenal, 4-oxononenal, malondialdehyde, and acrolein, and their influence on protein structures. Furthermore, we will examine inducing agents of cellular functioning, as well as intercellular signaling. These lipid peroxidation products can form adducts with a variety of proteins with different functions in the body, including proteins within skin cells and cells of the immune system. This is especially true in autoimmune diseases such as psoriasis. For example, these changes concern proteins involved in maintaining redox homeostasis or pro-inflammatory signaling. Therefore, the formation of such adducts should attract attention, especially during the design of preventive cosmetics or anti-psoriasis therapies.

摘要

银屑病是最常见的免疫介导性皮肤病之一,其特征是皮肤出现大量银屑病皮损,这是由于表皮细胞过度增殖和角化所致。这些角朊细胞代谢紊乱是由与免疫系统细胞(包括淋巴细胞)的病理性相互作用引起的,在银屑病中,淋巴细胞也负责全身炎症。这伴随着氧化应激,促进了脂质过氧化产物的形成,包括反应性醛和异前列腺素,它们是额外的促炎信号分子。因此,本综述重点强调了在银屑病发展过程中脂质过氧化产物(包括 4-羟壬烯醛、4-氧壬烯醛、丙二醛和丙烯醛)水平上发生的变化,以及它们对蛋白质结构的影响。此外,我们还将研究细胞功能的诱导剂以及细胞间信号转导。这些脂质过氧化产物可以与体内各种具有不同功能的蛋白质形成加合物,包括皮肤细胞和免疫系统细胞内的蛋白质。在自身免疫性疾病如银屑病中尤其如此。例如,这些变化涉及参与维持氧化还原稳态或促炎信号转导的蛋白质。因此,形成这种加合物应该引起关注,特别是在设计预防化妆品或抗银屑病疗法时。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab0e/10195986/e7607bccd1f2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab0e/10195986/3347d2d59d90/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab0e/10195986/e7607bccd1f2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab0e/10195986/3347d2d59d90/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab0e/10195986/e7607bccd1f2/gr1.jpg

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