ArticleAdvanced healthcare materials2026
Source-Dependent Mitochondrial Transplantation Drives Schwann Cell Bioenergetic Reprogramming and Peripheral Nerve Regeneration.
Article in Advanced healthcare materials, 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
10 authors.
Funding
Abstract
Following peripheral nerve injury (PNI), metabolic reprogramming of Schwann cells (SC) plays a critical role in axonal regeneration and functional recovery. Although mitochondrial transplantation (MT) has been proposed as a potential therapeutic strategy, it remains unclear whether its effect is limited to transient energy supplementation. We systematically compared the differential effects of mitochondria derived from human induced pluripotent stem cells (iPSCs, iP-MT) and induced mesenchymal stem cells (iMSCs, iM-MT) on regulating SC metabolism and promoting peripheral nerve regeneration. The results showed that exogenous mitochondria were efficiently taken up by SCs, not only increasing ATP production and mitochondrial membrane potential but also reshaping the metabolic distribution between glycolysis and oxidative phosphorylation. This remodeling promoted cell proliferation, migration, and neurotrophic function, while enhancing antioxidant capacity. In a rat sciatic nerve injury model, MT significantly improved axonal regeneration, remyelination, and the recovery of sensory and motor functions. Notably, iM-MT demonstrated stronger metabolic adaptability and therapeutic efficacy. MT reduced ROS accumulation, increased ATP production, and attenuated apoptosis under oxidative stress. This study reveals that MT promotes nerve repair by driving metabolic reprogramming rather than merely providing temporary energy, offering a new theoretical basis for optimizing the selection of mitochondrial donors.
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.