Evidence map›Paper›PMID 41769866›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Promotion of DFU Wound Healing via BRG1-COL16A1 Axis in Fibroblasts.

Penghui Wang, Jiaming Sun, Ying Wang, Bichen Ren, Yuxin Liu, Yunhan Liu, Liang Chen, Lu Yu, Tao Dai, Li Yu and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

11 authors.

Penghui WangDepartment of Vascular Surgery, Institute of Vascular Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0002-7356-8401
Jiaming SunDepartment of Plastic & Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ying WangChildren's Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Bichen RenDepartment of Vascular Surgery, Institute of Vascular Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Yuxin LiuDepartment of Plastic & Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yunhan LiuDepartment of Plastic & Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Liang ChenDepartment of Vascular Surgery, Institute of Vascular Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Lu YuDepartment of Vascular Surgery, Institute of Vascular Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Tao DaiDepartment of Wound Reconstructive Surgery, Tongji Hospital of Tongji University, Shanghai, China.
Li YuDepartment of Plastic & Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zhihui DongDepartment of Vascular Surgery, Institute of Vascular Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0002-3754-2458

Funding

Science and Technology Commission of Shanghai Municipality 23DZ2203200
6 · The paper itself

Abstract

Diabetic foot ulceration (DFU) imposes major global health burdens due to high morbidity and recurrence rates. Current therapies (debridement and offloading) show limited efficacy, highlighting the need to uncover molecular mechanisms of diabetic wound repair. Multi-omics analyses of DFU and healthy skin identify fibroblast-derived COL16A1 as a wound healing mediator. In vitro, COL16A1 overexpression or knockdown in fibroblasts is employed to assess its regulatory effects on cellular function and collagen secretory capacity. In vivo, localized adenoviral delivery of COL16A1 is administered to evaluate its therapeutic impact on wound closure in diabetic mice. DNA pull-down plus LC-MS/MS, ChIP-qPCR, and luciferase reporter assays are systematically implemented to delineate the upstream regulatory mechanism of COL16A1 expression. Transcriptomic profiling of skin specimens identifies fibroblast-derived COL16A1 as a key regulatory gene in DFU repair. Subsequent in vitro and in vivo experiments demonstrate COL16A1 enhances fibroblast activation and restores normal repair processes in diabetic wounds. Notably, Brahma-related gene 1 (BRG1) is identified as the key transcription factor governing COL16A1 expression. BRG1 directly binds to the COL16A1 promoter, upregulating its transcription and thereby accelerating diabetic wound healing. BRG1-COL16A1 axis is a critical regulatory pathway and proposes novel therapeutic targets for chronic diabetic wounds.

Indexed as

Diabetic FootDNA HelicasesFibroblastsNuclear ProteinsTranscription FactorsWound HealingAnimalsDisease Models, AnimalHumansMaleMiceDNA HelicasesNuclear ProteinsSMARCA4 protein, humanSmarca4 protein, mouseTranscription FactorsBRG1COL16A1DFUFibroblastWound Repair

Identifiers

PMID41769866
PMCPMC13159164

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.