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荟萃分析和转录组分析表明，NKRF 和 ZBTB17 调控 NF-κB 信号通路，共同参与阿尔茨海默病和动脉粥样硬化的分子机制。

Meta-analysis and transcriptomic analysis reveal that NKRF and ZBTB17 regulate the NF-κB signaling pathway, contributing to the shared molecular mechanisms of Alzheimer's disease and atherosclerosis.

机构信息

Department of Cardiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.

Laboratory Animal Science of China Medical University, Shenyang, Liaoning, China.

出版信息

CNS Neurosci Ther. 2024 May;30(5):e14683. doi: 10.1111/cns.14683.

DOI:10.1111/cns.14683
PMID:38738952
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11090078/
Abstract

INTRODUCTION

Alzheimer's disease (AD) and atherosclerosis (AS) are widespread diseases predominantly observed in the elderly population. Despite their prevalence, the underlying molecular interconnections between these two conditions are not well understood.

METHODS

Utilizing meta-analysis, bioinformatics methodologies, and the GEO database, we systematically analyzed transcriptome data to pinpoint key genes concurrently differentially expressed in AD and AS. Our experimental validations in mouse models highlighted the prominence of two genes, NKRF (NF-κB-repressing factor) and ZBTB17 (MYC-interacting zinc-finger protein 1).

RESULTS

These genes appear to influence the progression of both AD and AS by modulating the NF-κB signaling pathway, as confirmed through subsequent in vitro and in vivo studies.

CONCLUSIONS

This research uncovers a novel shared molecular pathway between AD and AS, underscoring the significant roles of NKRF and ZBTB17 in the pathogenesis of these disorders.

摘要

简介

阿尔茨海默病（AD）和动脉粥样硬化（AS）是在老年人群中广泛观察到的两种疾病。尽管它们很常见，但这两种疾病之间的潜在分子联系还不是很清楚。

方法

我们利用荟萃分析、生物信息学方法和 GEO 数据库，系统地分析了转录组数据，以确定在 AD 和 AS 中同时差异表达的关键基因。我们在小鼠模型中的实验验证突出了两个基因，NKRF（NF-κB 抑制因子）和 ZBTB17（MYC 相互作用的锌指蛋白 1）的重要性。

结果

这些基因似乎通过调节 NF-κB 信号通路来影响 AD 和 AS 的进展，这一点通过随后的体外和体内研究得到了证实。

结论

这项研究揭示了 AD 和 AS 之间的一种新的共同分子途径，强调了 NKRF 和 ZBTB17 在这些疾病发病机制中的重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35ee/11090078/edd18811d36c/CNS-30-e14683-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35ee/11090078/37cf1490efb6/CNS-30-e14683-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35ee/11090078/74f94d30796a/CNS-30-e14683-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35ee/11090078/0ba3fe328872/CNS-30-e14683-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35ee/11090078/cf2ab61b145a/CNS-30-e14683-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35ee/11090078/b4456d4026fb/CNS-30-e14683-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35ee/11090078/edd18811d36c/CNS-30-e14683-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35ee/11090078/37cf1490efb6/CNS-30-e14683-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35ee/11090078/74f94d30796a/CNS-30-e14683-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35ee/11090078/0ba3fe328872/CNS-30-e14683-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35ee/11090078/cf2ab61b145a/CNS-30-e14683-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35ee/11090078/b4456d4026fb/CNS-30-e14683-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35ee/11090078/edd18811d36c/CNS-30-e14683-g004.jpg

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