ArticleExperimental hematology2025
Mitochondrial retention and autophagy dysregulation drive oxidative stress in sickle cell disease erythrocytes.
Article in Experimental hematology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Targeting erythroid cell-derived asparagine inhibits alloimmunization in sickle cell disease.Blood advances · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Sickle cell disease (SCD) is an inherited blood disorder caused by a mutation in the β-globin gene, leading to hemoglobin polymerization under low oxygen conditions. This results in sickle-shaped red blood cells (erythrocytes), hemolysis, severe acute and chronic pain, and shortened erythrocyte lifespan. The severity of disease in SCD is linked to the type of hemoglobin mutation, with hemoglobin-SS genotype (HbSS) causing more frequent and severe than hemoglobin-SC genotype (HbSC). We previously identified mitochondrial retention and excessive reactive oxygen species (ROS) production in SCD erythrocytes. Here, we report that patients with SCD with the HbSS exhibit significantly higher erythrocyte mitochondrial retention and ROS levels than those with the HbSC. Mitochondrial retention positively correlates with serum bilirubin and lactate dehydrogenase (LDH), particularly in hydroxyurea-naïve patients. Gene expression analysis using a human autophagy array revealed upregulation of SNCA, GABARAP, GABRAPL2, MAP1LC3B, and CTSB in erythrocyte precursor cells from patients with SCD experiencing severe pain. Immunoblot analyses further confirmed accumulation of gamma-aminobutyric acid type-A receptor-associated protein (GABARAP), GABARAPL1, GABARAPL2, cathepsin-B, and alpha-synuclein in circulating erythrocytes and plasma from patients with SCD compared with controls. Our findings suggest a potential link between dysregulated autophagy proteins and erythrocyte mitochondrial retention in patients with SCD, opening new avenues for therapeutic interventions targeting these proteins to mitigate SCD pathogenesis.
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.