ArticleBlood advances2025
Cellular and biochemical heterogeneity contributes to the phenotypic diversity of transfusion-dependent β-thalassemia.
Article in Blood advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Acute pain transfusion reaction in a patient with thalassemia: In-depth characterization of short- and long-term phenotypes.Transfusion · 2026Article
- Red blood cell membrane proteome as a reporter of disease severity, transfusion impact and genetic background in transfusion-dependent β-thalassaemia.British journal of haematology · 2026Article
- Serum Metabolomic Signatures Indicate Oxidative Membrane Lipid Remodeling in β-Thalassemia.Metabolites · 2026Article
- Short- and long-term effects of transfusion in β-thalassemia: a longitudinal study of transfusion efficiency factors.Blood advances · 2026Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
26 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractTransfusion-dependent thalassemia (TDT) is a type of protein aggregation disease. Its clinical heterogeneity imposes challenges in effective management. Red blood cell (RBC) variables may be clinically relevant as mechanistic parts or tellers of TDT pathophysiology. This is a cross-sectional study of RBC and plasma physiology in adult patients with TDT vs healthy control. TDT plasma was characterized by increased protein carbonylation, antioxidants, and larger than normal extracellular vesicles. RBCs were osmotically resistant but prone to oxidative hemolysis. They overexposed phosphatidylserine and exhibited pathologically low proteasome proteolytic activity (PPA), which correlated with metabolic markers of the disease. RBC ultrastructure was distorted, with splenectomy-related membrane pits of 300 to 800 nm. Plasma metabolomics revealed differences in heme metabolism, redox potential, short-chain fatty acids, and nitric oxide bioavailability, but also in catecholamine pathways. According to coefficient of variation assessment, hemolysis, iron homeostasis, PPA, and phosphatidylserine exposure were highly variable among patients, as opposed to RBC fragility and plasma antioxidants, amino acids, and catecholamines. Sex-based differences were detected in hemolysis, redox, and energy variables, whereas splenectomy-related differences referred to thrombotic risk, RBC morphology, and plasma metabolites with neuroendocrine activity. Hepcidin varied according to oxidative hemolysis and metabolic markers of bacterial activity. Patients with higher pretransfusion hemoglobin levels (>10 g/dL) presented mildly distorted profiles and lower membrane-associated PPA, whereas classification by severity of mutations revealed different levels of hemostasis, inflammation, plasma epinephrine, hexosamines, and methyltransferase activity markers. The currently reported heterogeneity of cellular and biochemical features probably contributes to the wide phenotypic diversity of TDT at clinical level.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.