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Novel loci and biomedical consequences of iron homoeostasis variation.
Commun Biol
December 2024
BHF Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.
Iron homoeostasis is tightly regulated, with hepcidin and soluble transferrin receptor (sTfR) playing significant roles. However, the genetic determinants of these traits and the biomedical consequences of iron homoeostasis variation are unclear. In a meta-analysis of 12 cohorts involving 91,675 participants, we found 43 genomic loci associated with either hepcidin or sTfR concentration, of which 15 previously unreported.
View Article and Find Full Text PDFIron Homeostasis-Related Parameters and Hepcidin/Ferritin Ratio: Emerging Sex-Specific Predictive Markers for Metabolic Syndrome.
Metabolites
August 2024
Medical Biochemistry and Molecular Biology Department, Faculty of Medicine, Suez Canal University, Ismailia 41522, Egypt.
Metabolic syndrome (MetS) is a worldwide public health challenge. Accumulating evidence implicates elevated serum ferritin and disruptions in iron metabolism as potential elements linked to an increased risk of MetS. This study investigates the relationship between iron homeostasis-including hepcidin levels, serum iron concentration, unsaturated iron-binding capacity (UIBC), and the hepcidin/ferritin (H/F) ratio-and MetS.
View Article and Find Full Text PDFLack of Hfe and TfR2 in Macrophages Impairs Iron Metabolism in the Spleen and the Bone Marrow.
Int J Mol Sci
August 2024
Department of Clinical and Biological Sciences, University of Turin, 10126 Turin, Italy.
Article Synopsis
- - Iron is crucial for various metabolic functions in mammals, with its levels regulated primarily by hepcidin, influenced by proteins like Hfe and TfR2 found in macrophages involved in iron storage and delivery.
- - Mice lacking Hfe in macrophages show mild iron deficiency and increased production of the iron exporter Ferroportin 1 (Fpn1), affecting their iron metabolism and immune responses, particularly in aged subjects.
- - The study found that silencing Hfe and TfR2 in macrophages impacted iron levels in serum and liver, with notable differences in iron gene transcription and protein levels between adult and aged mice, highlighting the role of these proteins in regulating iron homeostasis and Erythropoietin
The role of TMPRSS6 gene polymorphism in iron resistance iron deficiency anaemia (IRIDA): a systematic review.
Ann Hematol
April 2024
Department of Pharmacology, Post Graduate Institute of Medical Education & Research (PGIMER), 4Th Floor, Research Block B, Chandigarh, India, 160012.
Iron resistance iron deficiency anaemia is a rare autosomal recessive disorder characterized by hypochromic microcytic anaemia, low transferrin saturation and inappropriately high hepcidin levels. The aetiology of this condition is rooted in genetic variations within the transmembrane serine protease 6 (TMPRSS6) genes, responsible for encoding matriptase-2, a pivotal negative regulator of hepcidin. We conducted a systematic search across four electronic databases, yielding 538 articles in total out of which 25 were finally included and were preceded further, aiming to prognosticate prevalent single nucleotide polymorphisms (SNPs) and detrimental genetic alterations.
View Article and Find Full Text PDFBiological variation of inflammatory and iron metabolism markers in high-endurance recreational athletes; are these markers useful for athlete monitoring?
Clin Chem Lab Med
April 2024
Laboratory Medicine Department, La Paz University Hospital, Madrid, Spain.
Objectives: To deliver biological variation (BV) data for serum hepcidin, soluble transferrin receptor (sTfR), erythropoietin (EPO) and interleukin 6 (IL-6) in a population of well-characterized high-endurance athletes, and to evaluate the potential influence of exercise and health-related factors on the BV.
Methods: Thirty triathletes (15 females) were sampled monthly (11 months). All samples were analyzed in duplicate and BV estimates were delivered by Bayesian and ANOVA methods.
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