ArticlebioRxiv : the preprint server for biology2025
Type 2 diabetes Reprograms Bone Marrow Hematopoiesis and Dysregulates Immune Signaling in Response to Stroke.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Type 2 diabetes mellitus (T2DM) worsens stroke outcomes, but the underlying mechanisms linking T2DM to systemic immune dysfunction remain unclear. We investigated whether T2DM alters bone marrow (BM) hematopoiesis and dysregulate immune signaling following ischemic stroke in mice. Single-cell RNA sequencing, GeoMx digital spatial profiling (DSP), nCounter, and flow cytometry were used to analyze BM cells from control (db/+, Ctrl) and diabetic (db/db, T2DM) mice underwent experimental stroke or sham surgery. Diabetes caused marked structural remodeling of BM, with reduced cellularity and imbalance of hematopoietic lineages. Pseudotime trajectory analysis revealed impaired differentiation and maturation signatures of hematopoietic progenitor cells (HPC1) and granulocytes, and overactivation toward monocytes in diabetes after stroke. CellChat analysis demonstrated reorganization of intercellular communication, with hematopoietic progenitor cells (HPC1) and monocytes emerging as dominant signaling hubs through upregulated MIF, SIRP, and THBS pathways. AUCell enrichment indicated increased glycolysis and oxidative phosphorylation but reduced interferon-γ (IFN-γ) signaling, reflecting metabolic activation coupled with immune dysregulation. DSP and nCounter further confirmed upregulation of genes in the MIF, SIRP and THBS pathways in CD115
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.