ReviewMolecular neurobiology2025
EVs from Stem Cells Improve Mitochondrial Dysfunction in Neuronal Disorders.
Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
- Vitamin D Promotes Neuronal Survival via Nrf2 Upregulation in D-Galactose-Induced Mice: An In-Vivo and In-Silico Study.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- DJ-1 in the Neuro-cutaneous Aging Axis: Unifying Pathways of Parkinson's Disease Neurodegeneration, Progression, and Redox-Based Therapeutic Strategies for Healthy Longevity.Molecular neurobiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction is a critical pathological trait of numerous neurodegenerative and inflammatory central nervous system (CNS) disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). Cellular stressors can directly modulate mitochondrial metabolism and increase the production of reactive oxygen species (ROS), thereby triggering mitochondrial retrograde signaling that alters nuclear gene expression and promotes the release of deleterious signal components into the cytoplasm. These processes contribute to neuronal injury and the progression of disease pathology. Emerging evidence underlines the therapeutic potential of extracellular vesicles (EVs) derived from stem cells such as mesenchymal stem cells (MSCs), neuronal stem cells (NSCs), and induced pluripotent stem cells (iPSCs) in reversing mitochondrial dysfunction. These nanoscale vesicles, which encapsulate transcription factors, nucleic acids, proteins, lipids, and even mitochondria, facilitate intercellular communication and influence the biological behaviour of recipient cells. Notably, stem cell-derived EVs have been shown to enhance mitochondrial function by improving the maximal oxygen consumption rate and spare respiratory capacity in injured neuronal cells. The molecular cargo within EVs, including miR-21, miR-29, and antioxidant enzymes, has been implicated in regulating mitochondrial biogenesis, reducing oxidative stress, and modulating pathways associated with apoptosis, mitophagy, and energy metabolism. Importantly, EVs can cross the blood-brain barrier (BBB), offering a minimally invasive strategy for targeted CNS delivery. In conclusion, stem cell-derived EVs represent a promising, cell-free therapeutic approach to restoring mitochondrial homeostasis and preventing neuronal disorders.
Indexed as
Identifiers
41417199What 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.