ArticleAnnals of hematology2025
Genetic biomarkers and crucial cell subsets of iron metabolism in Beta-Thalassemia: insights from bioinformatics and experimental validation.
Article in Annals of hematology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Approximately 1.5% of individuals with hemoglobin disorders carry the β-thalassemia gene variant, impacting around 40,000 newborns annually. Given the incomplete understanding of β-thalassemia pathogenesis, there is an urgent need to identify effective biomarkers to advance research, diagnosis, and treatment. This study aims to identify potential biomarkers for two key purposes: (1) diagnosing transfusion-dependent β-thalassemia (TDT) and (2) detecting iron overload complications, with a focus on functional markers that reflect iron metabolism dysregulation in TDT. This study integrates transcriptomic data from the Genome Sequence Archive dataset (CRA003639) with bioinformatics analysis to identify potential biomarkers associated with β-thalassemia. Subsequently, Hbb-bs and Hbb-bt double knockout mice were used to establish a β-thalassemia model, while C57BL/6JCya mice served as the control group, to validate the identified biomarkers through animal experiments. Seventeen reliable cell subsets were identified through rigorous annotation and screening. Quantitative analysis revealed a decreased proportion of immune cells (natural killer [NK] cells, T cells, macrophages, neutrophils, and monocytes) and an increased proportion of erythroid cells in the β-thalassemia group. Cell subset analysis focused on subsets that closely communicated with erythroid cells. Enrichment analysis of driver genes in these subsets revealed iron metabolism-related pathways in Erythroid_02 and Erythroid_03, and a ferroptosis-related pathway in Erythroid_05. Thalassemia model mice exhibited stronger iron ion fluorescence signals in primary hepatocytes, increased levels of total iron, Fe
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