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Exploring CACNA1H as a potential candidate biomarker for calcific aortic valve disease
Jun Chen1,2, Liusheng Wang1,2, Wenyan Li1,2
1State Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Insights
This study identifies CACNA1H as a key gene in calcific aortic valve disease (CAVD) progression. Inhibiting CACNA1H reduces valve calcification by impacting the NF-κB pathway, offering a potential therapeutic target for CAVD.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Genetics
Background:
- Calcific aortic valve disease (CAVD) is a common cardiovascular condition linked to significant mortality.
- Mechanical stress is a critical factor in CAVD pathogenesis, necessitating research into mechanosensitive ion channel-related genes (MICRGs).
Purpose of the Study:
- To identify key genes involved in CAVD pathogenesis using transcriptomic data.
- To investigate the role of CACNA1H in CAVD progression and its potential as a therapeutic target.
Main Methods:
- Differential gene expression analysis of CAVD patient data (GSE83453).
- Weighted gene co-expression network analysis (WGCNA) and MICRG identification.
- In vitro and in vivo experiments to assess CACNA1H inhibition effects.
- Analysis of the NF-κB signaling pathway.
Main Results:
- CACNA1H was identified as a candidate gene through the intersection of DEGs, WGCNA modules, and MICRGs.
- External datasets (GSE51472, GSE55492) validated CACNA1H as a significant gene in CAVD.
- CACNA1H inhibition was shown to alleviate CAVD progression by suppressing osteogenic response.
- CACNA1H inhibition attenuated P65 phosphorylation, impacting the NF-κB pathway.
Conclusions:
- CACNA1H plays a crucial role in CAVD pathogenesis by regulating the osteogenic response via the NF-κB pathway.
- CACNA1H inhibition presents a promising therapeutic strategy for managing CAVD.
- CACNA1H may serve as a valuable biomarker for CAVD diagnosis and prognosis.
Abstract:
Calcific aortic valve disease (CAVD) is a prevalent cardiovascular disorder characterized by calcium deposition in the aortic valve, associated with high morbidity and mortality. Mechanical stress plays a key role in its pathogenesis, highlighting the importance of identifying mechanosensitive ion channel-related genes (MICRGs). In this study, transcriptome data from GSE83453 of patients with CAVD and healthy controls were analyzed to identify differentially expressed genes (DEGs). Weighted gene co-expression network analysis (WGCNA) and MICRGs were used to pinpoint key genes. The intersection of DEGs, WGCNA modules, and MICRGs identified CACNA1H as a candidate gene. External validation with GSE51472 and GSE55492 confirmed these findings. Both in vitro and in vivo studies confirmed that CACNA1H inhibition alleviates CAVD progression by repressing the osteogenic response. Mechanistically, CACNA1H inhibition attenuated phosphorylation of P65, a key regulator of the NF-κB pathway. These results suggest that CACNA1H may serve as a promising biomarker and therapeutic target for CAVD.
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