Evidence map›Paper›PMID 40821102›Full record

ReviewAmerican journal of translational research2025

The role of apoptosis and its potential as a therapeutic target in inflammatory bowel disease associated with colorectal cancer.

Chuxin Zhang, Francis Atim Akanyibah, Xiu Wang, Fei Mao, Anquan Shang

Abstract readReview
In one paragraph

Review in American journal of translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. 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

5 authors.

Chuxin ZhangKey Laboratory of Medical Science and Laboratory Medicine of Jiangsu Province, School of Medicine, Jiangsu University Zhenjiang 212013, Jiangsu, P. R. China.
Francis Atim AkanyibahKey Laboratory of Medical Science and Laboratory Medicine of Jiangsu Province, School of Medicine, Jiangsu University Zhenjiang 212013, Jiangsu, P. R. China.
Xiu WangKey Laboratory of Medical Science and Laboratory Medicine of Jiangsu Province, School of Medicine, Jiangsu University Zhenjiang 212013, Jiangsu, P. R. China.
Fei MaoKey Laboratory of Medical Science and Laboratory Medicine of Jiangsu Province, School of Medicine, Jiangsu University Zhenjiang 212013, Jiangsu, P. R. China.
Anquan ShangDepartment of Laboratory Medicine, Lianyungang Clinical College, Jiangsu University Lianyungang 222006, Jiangsu, P. R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn's disease (CD), is a significant global health issue characterized by a complex etiology and high rates of recurrence. IBD increases the risk of acquiring colorectal cancer (CRC). CRC, the third leading cause of cancer worldwide, is becoming increasingly prevalent each year. Treatments targeting IBD and associated CRC do not yield effective results. One of the cell death processes associated with IBD pathogenesis is apoptosis. Although apoptosis helps maintain the intestinal barrier of the gut, excessive apoptosis is linked to the development of IBD and contributes to the growth and progression of CRC. In IBD, pro-apoptotic molecules are elevated, while they decrease in CRC. Therefore, therapies that inhibit pro-apoptotic molecules in IBD and enhance apoptosis in CRC may help prevent IBD and the associated CRC. This article reviews the mechanisms of apoptosis and its involvement in IBD and CRC. It also examines possible therapies, including gene and combination therapies that target apoptosis molecules and their signaling pathways in IBD and CRC.

Indexed as

Apoptosiscolorectal cancerinflammatory bowel diseasetherapy

Identifiers

PMID40821102
PMCPMC12351618

What OpenQuestion holds

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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.