Suppr超能文献

在感染性心肌抑制中,不确定性编码潜能转录本的比较转录组分析。

Comparative transcriptome analysis of transcripts of uncertain coding potential in septic myocardial depression.

机构信息

Department of Pediatrics, PICU, Shengjing Hospital of China Medical University, No. 36, SanHao Street, Shenyang City, 110004, Liaoning Province, People's Republic of China.

出版信息

BMC Cardiovasc Disord. 2021 Apr 8;21(1):166. doi: 10.1186/s12872-021-01973-z.

Abstract

BACKGROUND

Septic shock with myocardial depression is very common in intensive care units. However, the exact molecular mechanisms underlying sepsis-induced myocardial depression remain unclear. Whether the profiles of transcripts of uncertain coding potential (TUCPs) differ between patients with and without myocardial depression is also unknown. Our study aimed to find expression differences between groups of TUCPs and determine their potential functions in a preclinical model.

METHODS

We generated rat models of hypodynamic septic shock induced by lipopolysaccharide. A total of 12 rats were established and left ventricular tissue from each was collected. We performed RNA-seq to identify TUCPs in each sample. Transcripts with an corrected P value of < 0.05 were defined as differentially expressed (DE). We also performed GO terms and KEGG analysis to identify the potential functions of DE TUCPs.

RESULTS

A total of 4,851 TUCPs were identified in heart samples, 85 of which were expressed differently between the sepsis and control groups. Further bioinformatic analyses suggested that TUCPs play important roles in myocardial contraction, energy regulation, and metabolic processes, and are also involved in the regulation of several pathways.

CONCLUSION

Our results demonstrate that TUCPs both participate in and mediate the pathological process of myocardial depression. Our study improves the understanding of the basic molecular mechanisms underlying myocardial depression from a novel perspective.

摘要

背景

脓毒性休克伴心肌抑制在重症监护病房中很常见。然而,导致脓毒症引起心肌抑制的确切分子机制尚不清楚。是否不确定编码潜能(TUCPs)的转录本谱在有和没有心肌抑制的患者之间存在差异也尚不清楚。我们的研究旨在临床前模型中寻找 TUCP 组之间的表达差异,并确定其潜在功能。

方法

我们生成了由脂多糖诱导的低动力脓毒性休克的大鼠模型。共建立了 12 只大鼠,从每只大鼠的左心室组织中采集样本。我们进行了 RNA-seq 以鉴定每个样本中的 TUCPs。校正 P 值 < 0.05 的转录本被定义为差异表达(DE)。我们还进行了 GO 术语和 KEGG 分析,以确定 DE TUCPs 的潜在功能。

结果

在心脏样本中总共鉴定出 4851 个 TUCP,其中 85 个在脓毒症组和对照组之间表达不同。进一步的生物信息学分析表明,TUCPs 在心肌收缩、能量调节和代谢过程中发挥重要作用,并且还参与了几个途径的调节。

结论

我们的结果表明 TUCPs 既参与又介导了心肌抑制的病理过程。我们的研究从一个新的角度提高了对心肌抑制基本分子机制的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4e6/8028820/576d0a22c33a/12872_2021_1973_Fig1_HTML.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验