ArticleStem cell research & therapy2025
Protective effects of mouse bone marrow mesenchymal stem cell-derived extracellular vesicles on radiation-induced epididymal cells damage via USP44/RBM14 axis.
Article in Stem cell research & therapy, 2025. 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
8 authors.
Funding
Abstract
backgroundRadiation-induced damage to reproductive tissues presents a major clinical concern with potentially lasting functional consequences.
methodsHere, we investigate the protective function of extracellular vesicles derived from mouse bone marrow mesenchymal stem cells (mBMSCs-EVs) in mitigating ionizing radiation-induced injury in murine epididymal cells (mPC-1).
resultsWe demonstrate that mBMSC-EVs significantly enhance cell viability and reduce apoptosis, oxidative stress, and DNA damage in irradiated mPC-1 cells. Besides, we identify the deubiquitinase USP44 as a key mediator enriched in mBMSC-EVs, which confers radioprotection by stabilizing the RNA-binding protein RBM14 through deubiquitination for mPC-1 cells. Silencing USP44 in mBMSCs or their EVs abrogates these protective effects, leading to impaired DNA repair, increased apoptosis, oxidative stress, and disrupted cell cycle progression. Conversely, RBM14 overexpression partially restores cell survival and function, supporting its downstream role in this pathway.
conclusionOur findings reveal a novel USP44/RBM14 axis mediated by mBMSC-EVs that counteracts radiation injury, and suggest this mechanism as a promising therapeutic approach for protecting reproductive tissues from radiation-induced damage. Notably, these findings are primarily grounded in in vitro experiments utilizing an immortalized epididymal cell line; further in vivo validation and evaluation of clinical translatability are required prior to therapeutic application.
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.