ArticleCell death & disease2025
TNF-α-driven m6A modification disrupts the immunoregulatory function of MSCs by regulating HDAC5-dependent super-enhancers.
Article in Cell death & disease, 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
13 authors.
Funding
Abstract
Mesenchymal stem cells (MSCs) are extensively utilised to treat inflammatory diseases because of their strong immunosuppressive functions. However, these functions are strongly affected by the inflammatory microenvironment in vivo, which limits the therapeutic effect of MSCs. The present study demonstrated that TNF-α impairs the immunosuppressive effect of MSCs on T-cell proliferation. Mechanistically, TNF-α treatment decreased the expression of the H3 deacetylase HDAC5 and then led to increased super-enhancer (SE) signals and increased expression of leukaemia inhibitory factor (LIF), which results in the dysfunction of MSCs' immunosuppressive effect. Intravenous infusion of MSCs overexpressing HDAC5 increased therapeutic efficacy in SKG mice with inflammatory arthritis. Notably, TNF-α downregulated HDAC5 by promoting WTAP-mediated m6A modification of HDAC5 mRNAs, which are subsequently regulated by YTHDF2 to reduce mRNA stability. Our results reveal a synergistic epigenetic regulatory mechanism between SEs and m6A modification of MSC immunosuppressive functions and provide a novel strategy to promote the clinical therapeutic potential of MSC infusion in inflammatory diseases.
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.