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铜死亡在体外循环心脏手术后小儿先天性心脏病心肌免疫浸润中的潜在价值。

The potential value of cuprotosis in myocardial immune infiltration that occurs in pediatric congenital heart disease in response to surgery with cardiopulmonary bypass.

机构信息

Department of Cardiothoracic Surgery, Children's Hospital of Nanjing Medical University, Nanjing, China.

Department of Cardiothoracic Surgery, Nanjing Children's Hospital, Medical School of Nanjing University, Nanjing, China.

出版信息

Immun Inflamm Dis. 2023 Mar;11(3):e795. doi: 10.1002/iid3.795.

DOI:10.1002/iid3.795
PMID:36988255
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10013412/
Abstract

BACKGROUND

Cardiopulmonary bypass may cause malfunction in the myocardium. Cuproptosis is a novel cell death aggregating mitochondrial proteins. However, the research on cardiopulmonary bypass-caused heart tissue injury in immune infiltration and cuproptosis is limited.

METHOD

Immune infiltration, enrichment analysis, protein-protein interaction network, and medication prediction are applied to reanalysis differentially expressed genes and cuproptosis-related genes in gene expression omnibus data set GSE132176.

RESULTS

Seven cuproptosis related genes (PDHA1, LIPT1, LIAS, DLST, DLD, DLAT, and DBT) and dendritic cells and Th1 cells are involved in heart tissue injury in response to surgery with cardiopulmonary bypass.

CONCLUSIONS

Immune infiltration and cuproptosis are potential mechanisms by which cardiopulmonary bypass surgery may cause damage to heart tissue, which may be a new therapeutic target.

摘要

背景

体外循环可能导致心肌功能障碍。铜死亡是一种新型的聚集线粒体蛋白的细胞死亡方式。然而，关于体外循环引起的免疫浸润和铜死亡导致的心脏组织损伤的研究还很有限。

方法

应用免疫浸润、富集分析、蛋白质-蛋白质相互作用网络和药物预测对基因表达综合数据库 GSE132176 中差异表达基因和铜死亡相关基因进行重新分析。

结果

7 个铜死亡相关基因（PDHA1、LIPT1、LIAS、DLST、DLD、DLAT 和 DBT）以及树突状细胞和 Th1 细胞参与了体外循环手术引起的心脏组织损伤。

结论

免疫浸润和铜死亡可能是体外循环手术导致心脏组织损伤的潜在机制，这可能是一个新的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/fde4cb3b886c/IID3-11-e795-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/340573ee36ed/IID3-11-e795-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/481334aee6ac/IID3-11-e795-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/4eaf73c7758d/IID3-11-e795-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/05401680a73c/IID3-11-e795-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/ae5b356cbae4/IID3-11-e795-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/b0bf7f076df7/IID3-11-e795-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/7e91402eab6b/IID3-11-e795-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/16c53fb58799/IID3-11-e795-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/fde4cb3b886c/IID3-11-e795-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/340573ee36ed/IID3-11-e795-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/481334aee6ac/IID3-11-e795-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/4eaf73c7758d/IID3-11-e795-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/05401680a73c/IID3-11-e795-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/ae5b356cbae4/IID3-11-e795-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/b0bf7f076df7/IID3-11-e795-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/7e91402eab6b/IID3-11-e795-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/16c53fb58799/IID3-11-e795-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19fc/10013412/fde4cb3b886c/IID3-11-e795-g005.jpg

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Copper induces cell death by targeting lipoylated TCA cycle proteins.铜通过靶向脂酰化 TCA 循环蛋白诱导细胞死亡。
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