ArticleComprehensive physiology2026
Red Blood Cell Glycation Triggers In Vivo Cerebral Erythrophagocytosis in Adult Zebrafish in a Model Mimicking Hemorrhagic Stroke.
Article in Comprehensive physiology, 2026. 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.
- Red Blood Cell Glycation Triggers In Vivo Cerebral Erythrophagocytosis in Adult Zebrafish in a Model Mimicking Hemorrhagic Stroke.Comprehensive physiology · 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
8 authors.
Funding
Abstract
Hemorrhagic stroke, particularly intracerebral hemorrhage (ICH), is a highly lethal subtype of stroke, responsible for a poor prognosis and a high rate of disability. ICH is characterized by the extravasation of red blood cells (RBCs) into the central nervous system. Efficient clearance of RBC lysis products is critical. Erythrophagocytosis may serve as a key protective mechanism in mitigating secondary damage of ICH. Interestingly, diabetes is known to promote RBC glycation and to exacerbate the consequences of ICH. However, the link between glycation, RBC clearance and neurological outcomes after ICH is not clear. In this study, we aimed to decipher the role of glycated RBCs in ICH. For this, we used human RBCs glycated by methylglyoxal (MGO), an intermediate product of glycolysis recognized as one of the most potent glycating agents in humans. These glycated RBCs displayed altered morphology, reduced deformability capacity and increased eryptosis. We then proceeded to RBC microinjection into the brain parenchyma of Tg(mpeg1.1:mCherry) zebrafish allowing the visualization of both microglia and macrophages. Although the presence of RBCs in the parenchyma did not affect the increased recruitment of mpeg1.1-positive cells to the injection site compared to vehicle injection, RBC glycation significantly enhanced erythrophagocytosis. In conclusion, we established an innovative model of ICH, and we demonstrated enhanced RBC phagocytosis in the brain under glycated conditions. Further research is needed to understand the consequence of such process in ICH damage. Finally, our model may contribute to the identification of specific neurorestorative therapeutics aimed at improving brain plasticity after stroke in diabetic context.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.