通过激活 cGMP-PKG 信号通路，沉默 RGS7 可减轻心房颤动的进展。

IF 4.2 2区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-03-13 DOI:10.1016/j.bbadis.2025.167786

Hao Huang , Yan Xiong , Jie Zeng

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摘要

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Silencing RGS7 attenuates atrial fibrillation progression by activating the cGMP-PKG signaling pathway

Background

Atrial fibrillation (AF) is a common diagnosed heart disease that needs novel managements. This study aimed to seek potential biomarkers and underlying regulatory pathways associated with AF.

Methods

Differential expressed genes (DEGs) were identified from the Gene Expression Omnibus database, followed by a protein-protein interaction (PPI) network to discover hub genes. Principal components analysis (PCA) and receiver operating characteristic (ROC) curves were performed to evaluate the ability of hub genes to discriminate between AF and control. RGS7 was selected as a key hub gene, and genes co-expressed with RGS7 were identified for functional enrichment analysis. Further in vivo and in vitro experiments were conducted to investigate the effects of silencing RGS7 on AF and the potential pathway.

Results

We identified top 5 hub genes (RGS7, EGFR, RGS4, GNA13 and RGS11) from the PPI network. PCA showed these genes could distinguish between AF and control samples, with 100 % of the area under curve (AUC) values. Silencing RGS7 inhibited cell apoptosis, inflammation and oxidative stress, and increased mitochondrial membrane potential in angiotensin II (AngII)-treated HL-1 cells, while overexpression of RGS7 reversed the inhibitory effects of silencing RGS7 on AF. Additionally, silencing RGS7 improved cardiac function and decreased cardiac fibrosis in AF rats. The cGMP-PKG signaling pathway was screened as a potential signal transduction pathway, and silencing RGS7 increased the expression of PKG1, while KT5823 blocked the process.

Conclusion

Silencing RGS7 attenuates AF by activating the cGMP-PKG signaling pathway, which may offer directions for selecting biomarkers and regulatory pathways for AF.

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来源期刊

Biochimica et biophysica acta. Molecular basis of disease 生物-生化与分子生物学

CiteScore

12.30

自引率

0.00%

发文量

218

审稿时长

32 days

期刊介绍： BBA Molecular Basis of Disease addresses the biochemistry and molecular genetics of disease processes and models of human disease. This journal covers aspects of aging, cancer, metabolic-, neurological-, and immunological-based disease. Manuscripts focused on using animal models to elucidate biochemical and mechanistic insight in each of these conditions, are particularly encouraged. Manuscripts should emphasize the underlying mechanisms of disease pathways and provide novel contributions to the understanding and/or treatment of these disorders. Highly descriptive and method development submissions may be declined without full review. The submission of uninvited reviews to BBA - Molecular Basis of Disease is strongly discouraged, and any such uninvited review should be accompanied by a coverletter outlining the compelling reasons why the review should be considered.