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DOI 10.3389/fimmu.2024.1377409

Медицинская библиотека · Frontiers in immunology · 2024

CAP2 contributes to Parkinson's disease diagnosed by neutrophil extracellular trap-related immune activity.

Li Xiaohe, Luo Meiling, Xu Hangrui, Jia Lei, Liang Yanan, Xu Qianxi, Wang Yonghui

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

INTRODUCTION

Neutrophil extracellular traps (NETs) constitute a crucial element of the immune system, and dysfunction in immune responses is implicated in the susceptibility and progression of Parkinson's disease (PD). Nevertheless, the mechanism connecting PD and NETs remains unclear. This study aims to uncover potential NETs-related immune biomarkers and elucidate their role in PD pathogenesis.

METHODS

Through differential gene analysis of PD and NETs in GSE7621 datasets, we identified two PD subtypes and explored potential biological pathways. Subsequently, using ClusterWGCNA, we pinpointed pertinent genes and developed clinical diagnostic models. We then optimized the chosen model and evaluated its association with immune infiltration. Validation was conducted using the GSE20163 dataset. Screening the single-cell dataset GSE132758 revealed cell populations associated with the identified gene.

RESULTS

Our findings identified XGB as the optimal diagnostic model, with CAP2 identified as a pivotal gene. The risk model effectively predicted overall diagnosis rates, demonstrating a robust correlation between infiltrating immune cells and genes related to the XGB model.

DISCUSSION: In conclusions, we identified PD subtypes and diagnostic genes associated with NETs, highlighting CAP2 as a pivotal gene. These findings have significant implications for understanding potential molecular mechanisms and treatments for PD.

Для цитирования: Li Xiaohe, Luo Meiling, Xu Hangrui, Jia Lei, Liang Yanan, Xu Qianxi, Wang Yonghui. CAP2 contributes to Parkinson's disease diagnosed by neutrophil extracellular trap-related immune activity.. Frontiers in immunology. 2024. DOI: 10.3389/fimmu.2024.1377409.

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