Abstract
BACKGROUND: This study aims to investigate the role of ferroptosis in hypertrophic cardiomyopathy (HCM), a genetic disorder characterized by abnormal thickening of the heart muscle. The objective is to identify differentially expressed genes associated with ferroptosis in HCM and understand the potential molecular mechanisms underlying the disease. METHODS: Comprehensive genomic analysis was conducted to identify differentially expressed genes associated with ferroptosis in HCM. The analysis focused on TFRC, SCD, SLC2A1, EGR1, GDF15, SNCA, PLIN2, and NQO1 as hub genes regulating ferroptosis. Functional enrichment analysis was performed to uncover their involvement in pathways such as ferroptosis, ubiquinone biosynthesis, and HIF-1 signaling. In addition, immune cell infiltration patterns in HCM were explored, and associations between the hub genes and immune infiltration were identified. RESULTS: The analysis revealed TFRC, SCD, SLC2A1, EGR1, GDF15, SNCA, PLIN2, and NQO1 as hub genes involved in the regulation of ferroptosis in HCM. Functional enrichment analysis indicated their contribution to key pathways related to ferroptosis, ubiquinone biosynthesis, and HIF-1 signaling. Furthermore, associations between the hub genes and immune infiltration in HCM were observed. CONCLUSION: This study provides valuable insights into the molecular basis of HCM by identifying differentially expressed genes associated with ferroptosis. The findings suggest potential molecular mechanisms underlying the development of HCM. These findings contribute to a better understanding of HCM and may pave the way for the development of targeted therapies and improved diagnostic approaches for this debilitating cardiac disorder.