Evidence map›Paper›PMID 41667440›Full record

ReviewSignal transduction and targeted therapy2026

Ulcerative colitis: signaling pathways, therapeutic targets and interventional strategies.

Jinhao Jia, Ying Liu, Dan Wang, Zhaohai Pan, Qiusheng Zheng, Jun Lu, Chao Liang, Defang Li

Abstract readReview
In one paragraph

Review in Signal transduction and targeted therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
–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

19 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. UBE2L6 drives ulcerative colitis progression by promoting BIRC2 degradation and activating non-canonical NF-κB signalling.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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.

Jinhao Jia *Featured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, China.
Ying Liu *Featured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, China.
Dan WangFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, China.
Zhaohai PanFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, China.
Qiusheng ZhengFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, China.
Jun LuState Key Laboratory of Southwestern Chinese Medicine Resources, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China. ljaaa111@163.com.
Chao LiangDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, China. liangc@sustech.edu.cn.
Defang LiFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, China. lidefang@163.com.ORCID http://orcid.org/0000-0003-4151-9151

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82073313
6 · The paper itself

Abstract

Ulcerative colitis (UC) is the most common chronic inflammatory disease of the intestinal tract in clinical practice, and long-term chronic inflammation leads to repeated damage to and repair of the colonic mucosa, which may progress to malignancy through atypical hyperplasia. However, there are currently no fully targeted drugs for the treatment of UC. In this review, we discuss several cellular processes, such as autophagy, endoplasmic reticulum stress, mitochondrial dysfunction, macrophage polarization, ferroptosis and the Th/Treg cell balance, which are associated with the occurrence and development of UC. Many molecular targets and signaling pathways, such as nuclear factor kappa-B (NF-κB), phosphatidylinositol 3 kinase/protein kinase B (PI3K/AKT), Wnt/β-catenin, adenosine 5'-monophosphate-activated protein kinase (AMPK), toll-like receptor (TLR), Janus kinase/signal transducer and activator of transcription (JAK/STAT), long noncoding RNAs (lncRNAs), and microRNAs (miRNAs), play crucial roles in the progression of UC. We also summarize the common treatment strategies for UC, including lifestyle interventions, aminosalicylic acid preparations, corticosteroid drugs, biologics, fecal microbiota transplantation, and other drugs for symptomatic treatment. This review provides a detailed theoretical basis for the pathology and treatment of UC. Future research could focus on optimizing the treatment plan and achieving more precise and personalized treatment with multiple targets in multiple aspects.

Indexed as

Colitis, UlcerativeSignal TransductionAnimalsHumansMicroRNAsMicroRNAs

Identifiers

PMID41667440
PMCPMC12890998

What Socratic 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 Socratic graph.