ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2025
Impaired endothelial cell-derived CX3CL1-mediated macrophage efferocytosis in hypertrophic cardiomyopathy based on multi-omics analysis.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Integrative Transcriptomics and Machine Learning Identify Macrophage-Associated Biomarkers in Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2026Article
- Efferocytosis: unifying pathogenic hub in metabolic disorders-mechanistic landscapes, targeted therapies and translational bottlenecks.Frontiers in immunology · 2026Review
- Endothelial-specific genes TMTC1, RPS6KA2, and F8 are downregulated in hypertrophic cardiomyopathy.European journal of medical research · 2025Article
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7 authors.
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Abstract
backgroundClinical studies have demonstrated that multiple inflammatory related proteins are associated with hypertrophic cardiomyopathy (HCM). However, the precise role of these factors in the pathogenesis of HCM remains uncertain.
methodsThe link between inflammatory related proteins and HCM was analyzed using Mendelian randomization (MR), followed by bioinformatics to explore the role of inflammatory related proteins in HCM. In vivo and in vitro models of HCM were established to elucidate how inflammatory related proteins influence HCM progression.
resultsOur MR analysis revealed a negative correlation between the inflammation related protein CX3CL1 and HCM. Bioinformatics and in vivo data similarly demonstrated a reduction in CX3CL1 expression in HCM. CX3CL1 was found to be mainly expressed in cardiomyocytes and endothelial cells via the Human Protein Atlas database and its' expression in both cells was obviously downregulated after being treated by angiotensin-II. Importantly, functional characteristics and correlation analysis of CX3CL1 indicated that it was most closely associated with macrophages efferocytosis. Consequently, we examined the signature molecules (AXL, MERTK, and TYRO3) associated with efferocytosis, which revealed a significant decrease in their expression in HCM. Notably, recombinant mouse CX3CL1 (rm-CX3CL1) reversed this process.
conclusionsIn conclusion, CX3CL1-meidated impaired efferocytosis plays a critical role in the initiation and development of HCM, and modulation of CX3CL1 may prove advantageous in managing HCM progression.
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