ArticleJournal of translational medicine2026
3D-bioprinted mesenchymal stem cell-derived exosomes reprogram macrophages via PI3K/AKT to accelerate nerve regeneration.
Article in Journal of translational medicine, 2026. 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
11 authors.
Funding
Abstract
backgroundPeripheral nerve injury (PNI) regeneration involves complex immunoregulatory mechanisms, particularly M2 macrophage‑mediated immunomodulation. Promoting macrophage polarization toward the M2 phenotype represents a potential therapeutic strategy. Exosomes can create favorable microenvironments for tissue regeneration, but their clinical application is often limited by low concentration and purity. Three‑dimensional‑bioprinted exosomes (3D‑Exos) have recently gained attention due to their enhanced concentration and purity.
methodsIn this study, 3D‑Exos were applied to treat PNI. The regenerative effects of 3D‑Exos were compared with conventionally produced exosomes (2D‑Exos) in vivo. In vitro experiments, RNA sequencing, and miRNA microarray analyses were performed to investigate the underlying mechanisms. The mechanism was further validated in vitro and in vivo.
results3D‑Exos significantly enhanced nerve regeneration after PNI and outperformed 2D‑Exos. In vitro studies revealed that 3D‑Exos promoted macrophages polarization toward the M2 macrophages. RNA sequencing indicated that the PI3K/AKT pathway was activated by 3D‑Exos, and miRNA microarray analysis identified miR‑26b‑5p within 3D‑Exos as the key mediator targeting PTEN to activate PI3K/AKT signaling. Subsequently, M2 macrophages facilitated Schwann cell migration, elongation, and myelination, thereby accelerating nerve regeneration. Inhibition of the PI3K/AKT signaling pathway abolished the therapeutic effects of 3D-Exos on nerve regeneration after PNI.
conclusionsThis study elucidates a novel mechanism by which 3D‑Exos promote nerve regeneration through reprogramming macrophages polarization via the PI3K/AKT pathway. The work establishes a paradigm‑shifting therapeutic framework that integrates 3D-Exos with immunomodulatory strategies for the treatment of PNI.
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.