Evidence map›Paper›PMID 40386877›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

UTX Responds to Nanotopography to Suppress Macrophage Inflammatory Response by Remodeling H3K27me3 Modification.

Hengji Jia, He Zhang, Dingqiang Mo, Bo Xie, Hongdou Qiao, Tao Chen, Haoyue Song, Xinxin Xu, Sheng Yang

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Hengji JiaCollege of Stomatology, Chongqing Medical University, Chongqing, China.
He ZhangCollege of Stomatology, Chongqing Medical University, Chongqing, China.ORCID https://orcid.org/0009-0006-4348-5361
Dingqiang MoCollege of Stomatology, Chongqing Medical University, Chongqing, China.
Bo XieCollege of Stomatology, Chongqing Medical University, Chongqing, China.
Hongdou QiaoCollege of Stomatology, Chongqing Medical University, Chongqing, China.
Tao ChenCollege of Stomatology, Chongqing Medical University, Chongqing, China.
Haoyue SongCollege of Stomatology, Chongqing Medical University, Chongqing, China.
Xinxin XuCollege of Stomatology, Chongqing Medical University, Chongqing, China.
Sheng YangCollege of Stomatology, Chongqing Medical University, Chongqing, China.ORCID https://orcid.org/0000-0001-5062-6739

Funding

China Postdoctoral Science Foundation 2024MD764058National Natural Science Foundation of China 82170936National Natural Science Foundation of China 82371018National Natural Science Foundation of China U23A20447Natural Science Foundation of Chongqing CSTB2024NSCQ-MSX0525Postgraduate Research and Innovation Project of the Affiliated Stomatological Hospital of Chongqing Medical University KQY202302Program for Youth Innovation in Future Medicine, Chongqing Medical University W0079Project of Chongqing Medical University Graduate Tutor Team cqmudstd202203Scientific and Technological Research Program of Chongqing Municipal Education Commission KJZD-K202300402Special Grant for Chongqing Postdoctoral Research Project 2023CQBSHTB3129
6 · The paper itself

Abstract

Peri-implantitis is the leading cause of implant failure, primarily due to weak defense at the implant-soft tissue interface, which disrupts the local immune microenvironment. As an integral part of this microenvironment, the implant-tissue interface plays a critical role in shaping immune cell function. Thus, engineering the surface topography of implants has emerged as a novel strategy for sustained immunomodulation following implantation. This study investigated the mechanical regulation of macrophage function by nanopatterned topographies. Titanium nanotubes (TNTs) surfaces reduce the expression of phosphorylated myosin light chain (pMLC) and promote the retention of the UTX histone methyltransferase in the nucleus. This process attenuates the enrichment of the repressive H3K27me3 histone marker at the Abca1 gene locus, increasing Abca1 expression and suppressing inflammation. This study reveals the mechanosensitivity of UTX and provides a new target for the development of therapeutic strategies that integrate mechanical signaling and immune modulation.

Indexed as

Histone DemethylasesHistonesInflammationMacrophagesAnimalsHumansMiceNanotubesTitaniumHistone DemethylasesHistonesTitaniumUtx protein, mousehistone methylationmacropahgemechano‐immunologynanotopography

Identifiers

PMID40386877
PMCPMC12362724

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Registered trials

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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.