4.7 Article

Integrative analysis of genes reveals endoplasmic reticulum stress-related immune responses involved in dilated cardiomyopathy with fibrosis

Journal

APOPTOSIS
Volume 28, Issue 9-10, Pages 1406-1421

Publisher

SPRINGER
DOI: 10.1007/s10495-023-01871-z

Keywords

Endoplasmic reticulum stress; Dilated cardiomyopathy; Myocardial fibrosis; Bioinformatics; Immune cells

Ask authors/readers for more resources

Through analysis of microarray data, we identified potential biomarkers related to endoplasmic reticulum stress and explored their molecular mechanisms in myocardial fibrosis. Inflammatory immune imbalance and T-cell subsets play important roles in the progression of fibrosis. Additionally, we identified seven hub genes that may be involved in immune-related mechanisms.
Endoplasmic reticulum (ER) stress has been implicated in the mechanisms underlying the fibrotic process in dilated cardiomyopathy (DCM) and results in disease exacerbation; however, the molecular details of this mechanism remain unclear. Through microarray and bioinformatic analyses, we explored genetic alterations in myocardial fibrosis (MF) and identified potential biomarkers related to ER stress. We integrated two public microarray datasets, including 19 DCM and 16 control samples, and comprehensively analyzed differential expression, biological functions, molecular interactions, and immune infiltration levels. The immune cell signatures suggest that inflammatory immune imbalance may promote MF progression. Both innate and adaptive immunity are involved in MF development, and T-cell subsets account for a considerable proportion of immune infiltration. The immune subtypes were further compared, and 103 differentially expressed ER stress-related genes were identified. These genes were mainly enriched in neuronal apoptosis, protein modification, oxidative stress reaction, glycolysis and gluconeogenesis, and NOD-like receptor signaling pathways. Furthermore, the 15 highest-scoring core genes were identified. Seven hub genes (AK1, ARPC3, GSN, KPNA2, PARP1, PFKL, and PRKC) might participate in immune-related mechanisms. Our results offer a new integrative view of the pathways and interaction networks of ER stress-related genes and provide guidance for developing novel therapeutic strategies for MF.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available