ArticleRedox biology2026
hUCMSC mitochondrial EVs confer neuroprotection after ischemia by Tom1l2-mediated mitochondrial fusion and Crls1-cardiolipin axis reprogramming.
Article in Redox biology, 2026. 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.
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Who cites it
2 citing papers in PubMed.
- Mitochondrial homeostasis imbalance-triggered PANoptosis in traumatic brain and spinal cord injury: from mechanism to therapeutic strategies.Redox biology · 2026Review
- Advancing MSC-EV Therapies: Harnessing Preconditioning and Mito-EVs to Tackle Neuroinflammation and Neurodegeneration.Pharmaceutics · 2026Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction is a central driver of irreversible neuronal injury following ischemic stroke (IS); yet effective strategies to restore mitochondrial function and promote long-term neurological recovery remain limited. In this study, we demonstrate that mitochondrial extracellular vesicles derived from human umbilical cord mesenchymal stem cells (hUCMSC Mito-EVs) serve as a novel biotherapeutic vehicle capable of delivering functional mitochondria to damaged neurons. This process involves Target of Myb1-like 2 membrane trafficking protein (Tom1l2)-dependent membrane fusion between hUCMSC Mito-EVs and neuronal mitochondria, leading to the restoration of mitochondrial membrane potential and mitochondrial function. Mechanistically, Mito-EVs-mediated mitochondrial transfer upregulates cardiolipin synthase 1 (CRLS1), which preserves the inner mitochondrial membrane integrity and stabilizes respiratory chain complexes. The restoration of mitochondrial structure and function subsequently reduces reactive oxygen species production, suppresses pyroptosis, and promotes the recovery of neuronal metabolic and functional homeostasis. Collectively, these findings suggest that the Tom1l2-Crls1 axis serves as a key mediator of mitochondrial repair in hUCMSC Mito-EVs therapy, highlighting its promising potential as a targeted therapeutic strategy for neuronal protection following IS.
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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.