Evidence map›Paper›PMID 42018045›Full record

ArticleJournal of bioenergetics and biomembranes2026

A study on the mechanism of IGFBP-3 affecting autophagy to partially protect against inflammatory damage in inflammatory bowel disease.

Jiahui Liu, Jietong Ye, Shufang Ye, Lingling Chen, Yabi Zhu, Liming Wang, Kunqiang Yu, Xu Ma

Abstract read
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In one paragraph

Article in Journal of bioenergetics and biomembranes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Jiahui LiuDepartment of Gastroenterology, The First Affiliated Hospital of Lishui University, Lishui People's Hospital, No. 1188 Liyang Street, Liandu District, Lishui, Zhejiang, 323000, China.
Jietong YeDepartment of Gastroenterology, The First Affiliated Hospital of Lishui University, Lishui People's Hospital, No. 1188 Liyang Street, Liandu District, Lishui, Zhejiang, 323000, China.
Shufang YeDepartment of Gastroenterology, The First Affiliated Hospital of Lishui University, Lishui People's Hospital, No. 1188 Liyang Street, Liandu District, Lishui, Zhejiang, 323000, China.
Lingling ChenDepartment of Gastroenterology, The First Affiliated Hospital of Lishui University, Lishui People's Hospital, No. 1188 Liyang Street, Liandu District, Lishui, Zhejiang, 323000, China.
Yabi ZhuDepartment of Gastroenterology, The First Affiliated Hospital of Lishui University, Lishui People's Hospital, No. 1188 Liyang Street, Liandu District, Lishui, Zhejiang, 323000, China.
Liming WangDepartment of Gastroenterology, The First Affiliated Hospital of Lishui University, Lishui People's Hospital, No. 1188 Liyang Street, Liandu District, Lishui, Zhejiang, 323000, China.
Kunqiang YuCentral Laboratory, Lishui Second Hospital, Wenzhou Medical University, No. 69, Beihuan Road, Liandu District, Lishui City, Zhejiang Province, China. YuuKunQ0630@163.com.
Xu MaDepartment of Gastroenterology, The First Affiliated Hospital of Lishui University, Lishui People's Hospital, No. 1188 Liyang Street, Liandu District, Lishui, Zhejiang, 323000, China. MMaxXu0102@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Given the vital role of IGF-1 binding protein-3 (IGFBP-3) in inflammatory bowel disease (IBD), this study analyzed the mechanisms of IGFBP-3 affecting autophagy and inflammatory damage in IBD. IBD was induced in mice using 2,4,6-trinitrobenzenesulfonic acid. Mice were then treated with IGFBP-3 overexpression lentivirus, a Wnt/β-catenin pathway activator (HLY78), and an autophagy inhibitor (chloroquine). Body weight changes and disease activity index (DAI) scores within 7 days, as well as colon length and colon macroscopic visible damage scores, were recorded. Colon tissue morphology was observed using HE staining, with histological damage scored. ELISA was performed to determine tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-10 levels, and RT-qPCR and Western blot to measure IGFBP-3, Wnt, β-catenin, Axin2, LC3B II/I, and p62 levels in colon tissues. IBD mice exhibited decreased body weight and increased DAI scores within 7 days, along with a shortened colon length, increased macroscopic visible damage and histological damage scores, up-regulated TNF-α and IL-6 levels, and down-regulated IL-10 and IGFBP-3 levels in colon tissues. IGFBP-3 overexpression blocked the Wnt/β-catenin pathway and contributed to partial protection against inflammatory damage in colon tissues as well as promotion of autophagy in IBD mice. Inhibition of autophagy partially averted the protective effect of IGFBP-3 overexpression on inflammatory damage in IBD mice. IGFBP-3 disrupts the Wnt/β-catenin pathway and promotes autophagy, thereby partially protecting against inflammatory damage in IBD mice.

Indexed as

AutophagyInflammationInflammatory Bowel DiseasesInsulin-Like Growth Factor Binding Protein 3AnimalsMaleMiceWnt Signaling PathwayInsulin-Like Growth Factor Binding Protein 3AutophagyIGF-1 binding protein-3Inflammatory bowel diseaseInflammatory responseWntβ-catenin

Identifiers

PMID42018045

What OpenQuestion holds

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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.