ArticleJournal of translational medicine2025
Human umbilical MSC-derived exosomes improve intracerebral hemorrhage recovery via SIRT1-driven suppression of NF-κB/NOS2 signaling: coordinating microglial homeostasis and neuroprotection.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Intranasal administration of stem cells and their derivatives for neurological and respiratory disorders: a systematic review of human clinical trials.Frontiers in aging neuroscience · 2026Pooled it
- MSC-derived exosomes for hemorrhagic stroke: preclinical evidence and translational challenges.Frontiers in neurologyArticle
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
Intracerebral hemorrhage (ICH) remains a devastating neurological disorder with high mortality, driven primarily by uncontrolled neuroinflammation and secondary brain injury. Here, we show that human umbilical mesenchymal stem cell-derived exosomes (hUMSC-Exos) robustly promote functional recovery in a murine ICH model by reprogramming microglial biology and mitigating neuronal damage, via a mechanism dependent on the NAD⁺-dependent deacetylase SIRT1. Intranasal delivery of hUMSC-Exos enabled efficient uptake by perihematomal microglia, astrocytes, and neurons, reducing neuronal apoptosis and improving both sensorimotor and cognitive outcomes. Microglia-specific transcriptomic profiling revealed that hUMSC-Exos suppressed ICH-induced proinflammatory gene networks, particularly those governed by NF-κB/NOS2 signaling, while attenuating pathological microglial proliferation. Mechanistically, hUMSC-Exos upregulated SIRT1, which repressed NF-κB nuclear translocation and subsequent NOS2 expression. Pharmacological inhibition of SIRT1 with EX527 abrogated key beneficial effects of hUMSC-Exos: it reversed the suppression of microglial proliferation, restored neuronal apoptosis to ICH levels, and eliminated improvements in locomotor activity, anxiety-like behavior, and spatial learning/memory—assessed via open field and Morris water maze tests. Conversely, NOS2 blockade recapitulated the neuroprotective actions of hUMSC-Exos. Beyond anti-inflammatory effects, hUMSC-Exos promoted transcriptional programs linked to tissue remodeling and vascular regeneration, underscoring their dual role in mitigating injury and enhancing repair. Collectively, our study identifies a SIRT1-dependent axis through which stem cell-derived exosomes orchestrate microglial homeostasis and neuronal survival after ICH, establishing exosome-based therapy as a promising cell-free strategy for acute brain injury with translational potential.
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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.