ArticleApoptosis : an international journal on programmed cell death2026
BMSC-derived exosomal METTL3 synergizes with Sevoflurane to inhibit ferroptosis in pulmonary ischemia/reperfusion injury by enhancing USP7 N6-methyladenosine modification.
Article in Apoptosis : an international journal on programmed cell death, 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
6 authors.
Funding
Abstract
Inhibition of ferroptosis was shown to alleviate pulmonary ischemia/reperfusion (I/R) injury. This study aimed to investigate the synergistic effects of bone marrow mesenchymal stem cells (BMSC)-derived exosomal METTL3 and Sevoflurane (Sev) in alleviating pulmonary I/R injury through ferroptosis regulation. In our study, pulmonary I/R injury models were established in mice and lung microvascular endothelial cells (LMECs). Commercial kits were used to measure myeloperoxidase (MPO), glutathione (GSH), malondialdehyde (MDA), and iron content. Lipid peroxidation was determined using the BODIPY 581/591 C11 probe by flow cytometry. Total m6A modification was measured by the commercial kit and m6A dot blot, while m6A modification of USP7 mRNA was analyzed by MeRIP and polysome profiling. The interaction between proteins or RNAs was analyzed by Co-IP, FISH combined with immunofluorescence, RNA pull-down, RIP, or dual-luciferase reporter assay. We proved Sev preconditioning mitigated ferroptosis in pulmonary I/R injury by activating the Nrf2 pathway. Co-treatment with BMSC-derived exosomes potentiated the protective effects of Sev by promoting USP7-mediated Nrf2 deubiquitination modification. Mechanistically, BMSC-derived exosomal METTL3 promoted USP7 mRNA translation through YTHDC2-dependent m6A modification. Also, METTL3 knockdown in exosomes suppressed the Nrf2 pathway and exacerbated ferroptosis, while METTL3 overexpression showed opposite effects. YTHDC2 knockdown abolished these protective effects caused by METTL3-overexpressed exosomes. In conclusion, BMSC-derived exosomal METTL3 reinforced the protective effects of Sev by promoting USP7 mRNA translation via YTHDC2-dependent m6A modification. Upregulated USP7 subsequently facilitated Nrf2 deubiquitination, thereby inhibiting ferroptosis and protecting against pulmonary I/R injury.
Indexed as
Identifiers
42487045What 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.