ArticleInflammation2026
MAPK15 Attenuates Intestinal Epithelial Cell Senescence-Like Phenotype to Regulate Gut Homeostasis and Inflammation by Phosphorylating Suz12 to Suppress Drp1-Mediated Mitochondrial Fission Damage.
Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The senescence of intestinal epithelial cells (IECs) is closely associated with the development of ulcerative colitis (UC), but the underlying regulatory mechanism remains unclear. Although mitogen activated protein kinase 15 (MAPK15) has been shown to inhibit cellular senescence, its specific role in UC has not yet been clarified. This study investigates the role of MAPK15 in modulating IEC senescence during UC and explores the molecular mechanisms involved in this regulatory process. The senescence phenotype and MAPK15 expression in colon tissues from UC patients, dextran sodium sulfate (DSS)-induced UC mice, and DSS-induced NCM460 cells were detected by SA-β-Gal staining, immunohistochemistry (IHC) staining, and Western blot analysis. To further determine the molecular mechanism of the MAPK15/Suz12/Drp1 axis in UC, MAPK15 was overexpressed and Suz12 was silenced, and the underlying regulatory interactions were assessed using techniques including Co-immunoprecipitation (Co-IP), RIP-qPCR, and RNA pull-down. The results showed that the expressions of senescence-associated markers (p53, p16, and p21) and senescence-associated secretory phenotype (SASP) factors (IL-6, IL-8, and MMP-3) in IECs from UC patients and DSS-induced mice were upregulated, whereas the expression of MAPK15 was downregulated. Functional experiments further demonstrated that overexpression of MAPK15 alleviated DSS-induced intestinal inflammation, reduced cellular senescence-like phenotype, and suppressed Drp1-dependent mitochondrial fission. Mechanistically, MAPK15 enhanced the binding of Suz12 to Drp1 mRNA through phosphorylation of Suz12, which reduced the stability of Drp1 mRNA, and thereby inhibited Drp1-mediated mitochondrial fission damage. However, silencing of Suz12 reversed the protective effect induced by MAPK15 overexpression. In conclusion, these findings indicated that MAPK15 contributed to the inhibition of mitochondrial fission through regulation of the Suz12/Drp1 axis, thereby mitigating IEC senescence-like phenotype and suppressing the progression of UC. These results suggested that MAPK15 might serve as a potential therapeutic target for UC.Clinical Trial Number: Not applicable.
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.