Answers are grounded in this paper and cite their sources.
Bioinformatics analysis reveals 13 hub genes as promising diagnostic biomarkers for dilated cardiomyopathy, indicating roles in immune cell response.
Background: Dilated cardiomyopathy (DCM) is a primary cardiomyopathy of unknown etiology that is common in children and older adults. Nevertheless, the absence of noticeable symptoms and the lack of suitable biomarkers pose obstacles to the timely detection and management of DCM. Results: By comparing samples from dilated cardiomyopathy and controls, 629 differentially expressed genes (DEGs) were identified. Combined with WGCAN results, a total of 13 hub genes were identified by intersecting DEGs and oxidative stress (OS)-related modular genes.These hub genes included MVP, WISP1, LCP1, FTL, FCN1, PAPSS1, KRT14, SULT1C2, RARRES1, DIRAS3, AMPD3, F2RL1 and COL6A3. The analysis of the ROC curve showed a good predictive ability for DCM of these hub genes. Furthermore, enrichment analysis revealed that these hub genes have primarily participated in the process of transmembrane transport and nucleotide metabolism. The analysis of immune cell infiltration found significantly increased infiltration of activated B cells, natural killer cells, CD56dim natural killer cells, macrophages, and monocytes in the DCM group compared to the control group. Additionally, we validated the hub genes in an induced DCM mouse model and demonstrated the upregulation of MVP, WISP1, FTL, FCN1, and KRT14 in the DCM mice. Conclusion: The hub genes MVP, WISP1, FTL, FCN1, AMPD3, KRT14, and RARRES1 have the potential to serve as diagnostic biomarkers for DCM, offering novel insights into the clinical diagnosis.
No takes yet. Share an insight, caveat, or question.
Cao et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: