ArticleLung2026
USP10 from Human Umbilical Cord Mesenchymal Stem Cells-Derived Extracellular Vesicles Mediates SCL7A11 Deubiquitination in Epithelial Cells: A Key to Anti-ferroptosis and Anti-fibrosis in Pulmonary Fibrosis.
Article in Lung, 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
4 authors.
Funding
Abstract
objectivePulmonary fibrosis (PF) is a lethal lung disease distinguished by deteriorating pulmonary function. This study investigated whether human umbilical cord mesenchymal stem cells (HUMSCs) alleviate PF in mice by suppressing ferroptosis through ubiquitin-specific protease 10 (USP10)-mediated deubiquitination of solute carrier family 7 member 11 (SLC7A11).
methodsA bleomycin (BLM)-induced PF mouse model was established and treated with HUMSCs or Erastin. In vitro, BEAS-2B cells were challenged with BLM and co-cultured with HUMSCs, with further manipulations using si-SLC7A11, si-USP10, or oe-USP10. USP10 expression in the characterized HUMSCs-derived extracellular vesicles (EVs) were measured by western blot techniques. Lung edema, histopathology, fibrosis, collagen deposition, and hydroxyproline were assessed. Ferroptosis, cell viability, cell death, lipid peroxidation, SLC7A11/USP10 expression, and fibrosis were analyzed by CCK-8, lactate dehydrogenase, BODIPY 581/591 C11 staining, RT-qPCR, and western blot assays. USP10-SLC7A11 interaction, SLC7A11 ubiquitination, and protein stability were evaluated using Co-immunoprecipitation and cycloheximide chase assay.
resultsBLM-induced PF mice exhibited aggravated lung injury, enhanced fibrosis and ferroptosis, and reduced glutathione peroxidase 4, SLC7A11, and USP10 expression. USP10 was enriched in HUMSCs-EVs. HUMSCs significantly upregulated USP10, attenuated PF, and suppressed ferroptosis in vivo and in vitro. USP10 knockdown or SLC7A11 downregulation reversed the protective effects of HUMSCs. Mechanistically, BLM-induced downregulation of USP10 increased SLC7A11 ubiquitination and reduced its protein stability. In vivo experiments validated that HUMSCs-mediated USP10/SLC7A11 mitigated BLM-induced PF in mice by inhibiting ferroptosis.
conclusionsHUMSCs-EVs ameliorate BLM-induced PF by inhibiting ferroptosis through USP10-mediated deubiquitination of SLC7A11, highlighting a novel therapeutic mechanism for MSC-based therapy in PF.
Indexed as
Identifiers
42053831What 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.