2026-07-02 | Interleukin-1β and Glycolytic Enzyme Alterations in Beta-Thalassemia Major: Insights into Inflammation-Metabolism Crosstalk
Background: Beta-thalassemia major is characterized by chronic hemolytic anemia, ineffective erythropoiesis, and systemic iron overload, leading to metabolic and inflammatory alterations. Objective: This study investigated the relationship between serum interleukin-1β (IL-1β), key glycolytic enzymes (hexokinase [HK], pyruvate kinase [PK], phosphofructokinase [PFK]), and PFKP gene expression in beta-thalassemia major patients. Methods: A case-control study was conducted involving 42 beta-thalassemia major patients and 30 healthy controls. Serum levels of IL-1β, HK, PK, and PFK were measured using ELISA, while PFKP gene expression was assessed by RT-qPCR. Results: Patients exhibited significantly elevated IL-1β (41.34 ± 42.23 vs. 21.43 ± 26.45 pg/mL; p = 0.0276), HK (327.71 ± 282.40 vs. 131.47 ± 158.67 pg/mL; p = 0.0012), and PFK (1.83 ± 1.52 vs. 0.51 ± 0.53 ng/mL; p < 0.0001) compared to controls. Strong positive correlations were observed between IL-1β and glycolytic enzymes (r = 0.637-0.690, p < 0.0001). Conclusion: These findings demonstrate significant inflammation-metabolism crosstalk in beta-thalassemia major, suggesting that targeting inflammatory pathways may ameliorate metabolic disturbances in affected patients.
Open article ↗
2026-06-30 | The Adverse Effects of Thalassemia Treatments Including Blood Transfusion and Main Pharmacological Therapies
Beta-thalassemia major (β-TM) is a disorder which needs lifelong blood transfusions. Our aim was to examine the treatments side effects in thalassemic patients. Methods: 110 β-TM patients attending two centers were invited to the study. Those who consented were asked to complete a questionnaire. The questionnaire covered demographical information, used medications and their side effects. The data was analyzed using SPSS software version 14. Results: Data was collected between August 2008 and July 2009. Patients' age was 14.0±1.32 years. The duration of treatment was 11.3±7.5 years. Thalassemic patients received blood transfusions, deferoxamine and supportive medications. Number of medications, received by patients was 3.9±1.9. Hemosiderosis in heart (11%) and endocrine system (8%) were main blood transfusion side effects. A few had hepatitis B or C. Conclusion: Because of prevalence of side effects of therapies, reviewing and improving treatment protocol by designing new medicines with lower side effects and establishment of an adverse reactions team seemed necessary.
Open article ↗
2026-06-29 | Protection of Islet Beta Cells from Iron Overload-Induced Injury by Long Non-Coding RNA Maternally Expressed Gene 3.
Patients with beta-thalassemia major (β-TM) commonly present with abnormal glucose metabolism, and factors such as iron overload, chronic anaemia, hormonal imbalances, liver dysfunction and inflammation-associated insulin resistance are considered important contributors to pancreatic islet dysfunction. Long non-coding ribonucleic acids (lncRNAs) are increasingly recognised for their regulatory roles in cell apoptosis and glucose homeostasis. This study explores the function of the lncRNA, maternally expressed gene 3 (MEG3), in iron-induced islet β-cell injury. An iron-overload mouse model was induced via intraperitoneal injection of iron dextran. Iron deposition and tissue damage in the pancreas were evaluated using Prussian blue and hematoxylin and eosin staining, and MEG3 expression was quantified via reverse transcription polymerase chain reaction (RT-PCR). In vitro, MIN6 cells were transfected with MEG3 small interfering RNA to examine apoptosis via flow cytometry, and NF-kappa (ĸ)B signaling pathway activity was assessed by Western blotting. Histological staining confirmed significant iron deposition and structural damage in the pancreatic tissue of iron-overloaded mice. The RT-PCR analysis revealed a marked reduction of MEG3 expression in the pancreas (p<0.05). In vitro, MEG3 knockdown significantly increased apoptosis of MIN6 cells compared with controls. Western blot analysis showed an elevated level of NF-ĸB, indicating activation of the NF-ĸB signaling pathway in MEG3-silenced cells. These findings suggest that MEG3 downregulation may enhance islet β-cell apoptosis via NF-ĸB signaling under iron overload conditions. The MEG3 gene may play a protective role against iron-induced islet β-cell apoptosis, potentially involving modulation of the NF-ĸB pathway. This mechanism may contribute to islet dysfunction in patients with β-TM with iron overload.
Open article ↗
