Evidence map›Paper›PMID 39412701›Full record

ArticleActa diabetologica2025

Facilitation of diabetic wound healing by far upstream element binding protein 1 through augmentation of dermal fibroblast activity.

Shali Ou, Chao Sima, Zhihe Liu, Xiaojian Li, Bing Chen

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In one paragraph

Article in Acta diabetologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Shali Ou *Department of Burns and Plastic Surgery, Guangzhou Red Cross Hospital of Jinan University, No 369, Tongfu Middle Road, Guangzhou, Guangdong, China.
Chao Sima *Department of Burns and Plastic Surgery, Guangzhou Red Cross Hospital of Jinan University, No 369, Tongfu Middle Road, Guangzhou, Guangdong, China.
Zhihe LiuGuangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital of Jinan University, Guangzhou, China.
Xiaojian LiDepartment of Burns and Plastic Surgery, Guangzhou Red Cross Hospital of Jinan University, No 369, Tongfu Middle Road, Guangzhou, Guangdong, China.
Bing ChenDepartment of Burns and Plastic Surgery, Guangzhou Red Cross Hospital of Jinan University, No 369, Tongfu Middle Road, Guangzhou, Guangdong, China. lookforword@163.com.

Funding

Guangzhou Municipal Science and Technology Project 33122167
6 · The paper itself

Abstract

aimsDiabetes mellitus (DM) often leads to wound healing complications, partly attributed to the accumulation of advanced glycosylation end products (AGEs) that impair fibroblast function. Far Upstream Element Binding Protein 1 (FUBP1) regulates cell proliferation, migration, and collagen synthesis. However, the impact of FUBP1 on diabetic wound healing remains unknown. This study is designed to explore the function and mechanisms of FUBP1 in diabetic wound healing.

methodsEighteen Sprague-Dawley rats (weighing 220-240 g) were randomly assigned to three groups (n = 6): a control group (NC) of healthy rats, a model group (DM) of untreated diabetic rats, and a treatment group (DM + FUBP1) of diabetic rats accepting FUBP1 treatment. A 10 mm diameter circular full-thickness skin defect was created on the back of each rat. On days 1 and 7, rats in the treatment group received local injections of 5 µg FUBP1 protein at the wound site, whereas the control group and model group were administered saline. Wound healing was documented on days 0, 3, 7, 10, and 14, with tissue samples from the wound areas collected on day 14 for histological analysis, including H&E staining, Masson's trichrome staining, and immunohistochemistry. Western blot analysis was utilized to assess the expression of GSK-3β, Wnt3a, and β-catenin. In vitro, the effects of various concentrations of AGEs on cell viability and FUBP1 expression were examined in human dermal fibroblasts (HDF). Cells were genetically modified to overexpress FUBP1 using lentiviral vectors and were cultured for 48 h in media with or without AGEs. The impacts on fibroblast proliferation, migration, and Wnt/β-catenin signaling were evaluated using CCK-8, scratch assays, and Western blot analysis.

resultsAnimal investigation revealed that from day 7 onwards, the wound healing rate of the treatment group was higher than that of the model group but lower than the control group. On day 14, the wound healing rates were as follows: control group (0.97 ± 0.01), model group (0.84 ± 0.03), and treatment group (0.93 ± 0.01). These differences were statistically significant. Histological analysis indicates that FUBP1 promotes granulation tissue formation, re-epithelialization, and collagen deposition in treatment group. Additionally, FUBP1 protein expression decreased in dermal fibroblasts when exposed to AGEs. Overexpression of FUBP1 significantly enhanced fibroblast proliferation and migration, activating the Wnt/β-catenin pathway and mitigating the inhibitory effects of AGEs.

conclusionsOur results suggest that FUBP1 can be a promising therapeutic target for diabetic wound healing, potentially counteracting the detrimental effects of AGEs on dermal fibroblasts through the Wnt/β-catenin pathway.

Indexed as

DermisDiabetes Mellitus, ExperimentalDNA-Binding ProteinsDNA HelicasesFibroblastsRNA-Binding ProteinsWound HealingAnimalsCell MovementCell ProliferationHumansMaleRatsRats, Sprague-DawleySkinWnt Signaling PathwayDNA-Binding ProteinsDNA HelicasesRNA-Binding ProteinsAdvanced glycosylation end products (AGEs)Dermal fibroblastsDiabetic wound healingFar upstream element binding protein 1 (FUBP1)Wnt/β-catenin signaling

Identifiers

PMID39412701

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