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Gasdermin E (GSDME)-一种新的银屑病及其代谢并发症的潜在标志物:血清、尿液和组织的首次联合研究。

Gasdermin E (GSDME)-A New Potential Marker of Psoriasis and Its Metabolic Complications: The First Combined Study on Human Serum, Urine and Tissue.

机构信息

Department of Dermatology and Venereology, Medical University of Bialystok, 14 Zurawia St., 15-540 Bialystok, Poland.

Department of General Pathomorphology, Medical University of Bialystok, 13 Waszyngtona St., 15-269 Bialystok, Poland.

出版信息

Cells. 2023 Aug 26;12(17):2149. doi: 10.3390/cells12172149.

Abstract

Psoriasis is a frequent and incurable skin disease whose pathogenesis is still not fully understood. It is characterized by immune disturbances leading to hyperproliferation and improper differentiation of keratinocytes. Gasdermin E (GSDME) is a protein from the gasdermin family involved in the processes of inflammation and cell death based on apoptosis, necroptosis and pyroptosis. It has never been studied in psoriatics' sera or urine before. Our study enrolled 60 patients with psoriasis and 30 volunteers without dermatoses as controls. Serum and urinary GSDME concentrations were examined by ELISA and tissue expression of GSDME by immunohistochemistry. Serum GSDME concentration was significantly higher in patients than controls ( < 0.05). There were no differences in urinary GSDME concentrations between patients and controls. GSDME expression was significantly higher in the psoriatic plaque than non-lesional patients' skin and compared to controls (both < 0.001). There was no correlation between serum GSDME or its lesional expression and psoriasis severity, age or disease duration. GSDME serum concentration was significantly negatively correlated with BMI, triglycerides and glucose concentrations. The obtained results suggest the engagement of GSDME in psoriasis pathogenesis. It could potentially become a new non-invasive psoriasis marker. Considering its pro-apoptotic influence, GSDME could be compensatively elevated to direct cells towards apoptosis, whereas under other circumstances, it may lead to pyroptosis and sustain inflammation. GSDME may exert a protective influence on the metabolic complications in psoriasis which requires further studies.

摘要

银屑病是一种常见且无法治愈的皮肤病,其发病机制尚未完全阐明。它的特征是免疫紊乱导致角质形成细胞过度增殖和异常分化。Gasdermin E(GSDME)是一种gasdermin 家族的蛋白,参与炎症和细胞死亡过程,基于细胞凋亡、坏死性凋亡和细胞焦亡。以前从未在银屑病患者的血清或尿液中研究过它。我们的研究纳入了 60 名银屑病患者和 30 名无皮肤病的志愿者作为对照。通过 ELISA 检测血清和尿液 GSDME 浓度,通过免疫组织化学检测 GSDME 的组织表达。患者的血清 GSDME 浓度明显高于对照组(<0.05)。患者和对照组之间的尿 GSDME 浓度没有差异。银屑病斑块中的 GSDME 表达明显高于非病变患者的皮肤和对照组(均<0.001)。血清 GSDME 或其病变表达与银屑病严重程度、年龄或疾病持续时间之间没有相关性。血清 GSDME 浓度与 BMI、甘油三酯和血糖浓度呈显著负相关。所得结果表明 GSDME 参与了银屑病的发病机制。它可能成为一种新的非侵入性银屑病标志物。考虑到其促凋亡的影响,GSDME 可能会代偿性升高,以使细胞走向凋亡,而在其他情况下,它可能导致细胞焦亡并维持炎症。GSDME 可能对银屑病的代谢并发症产生保护作用,这需要进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c06/10486754/050f2df61635/cells-12-02149-g001.jpg

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