Evidence map›Paper›PMID 26823956›Full record

ReviewOxidative medicine and cellular longevity2016

Oxidative Stress and Carbonyl Lesions in Ulcerative Colitis and Associated Colorectal Cancer.

Zhiqi Wang, Sai Li, Yu Cao, Xuefei Tian, Rong Zeng, Duan-Fang Liao, Deliang Cao

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% of its field
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

97 citing papers in PubMed, 1 synthesis or guideline pooled it, 210 citations in OpenAlex.

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  16. Journal of inflammation research · 2025
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37 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 2 countries.

Zhiqi WangDepartment of Pharmacology, Division of Stem Cell Regulation and Application, State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan (Incubation), and Key Laboratory of Colleges and Universities in Hunan Province for Cytobiology and Molecular Biotechnology, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China.
Sai LiDepartment of Pharmacology, Division of Stem Cell Regulation and Application, State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan (Incubation), and Key Laboratory of Colleges and Universities in Hunan Province for Cytobiology and Molecular Biotechnology, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China.
Yu CaoDepartment of Medical Microbiology, Immunology & Cell Biology, Simmons Cancer Institute, Southern Illinois University School of Medicine, 913 N. Rutledge Street, Springfield, IL 62794, USA.
Xuefei TianDepartment of Pharmacology, Division of Stem Cell Regulation and Application, State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan (Incubation), and Key Laboratory of Colleges and Universities in Hunan Province for Cytobiology and Molecular Biotechnology, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China.
Rong ZengDepartment of Pharmacology, Division of Stem Cell Regulation and Application, State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan (Incubation), and Key Laboratory of Colleges and Universities in Hunan Province for Cytobiology and Molecular Biotechnology, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China.
Duan-Fang LiaoDepartment of Pharmacology, Division of Stem Cell Regulation and Application, State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan (Incubation), and Key Laboratory of Colleges and Universities in Hunan Province for Cytobiology and Molecular Biotechnology, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China.
Deliang CaoDepartment of Pharmacology, Division of Stem Cell Regulation and Application, State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan (Incubation), and Key Laboratory of Colleges and Universities in Hunan Province for Cytobiology and Molecular Biotechnology, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China; Department of Medical Microbiology, Immunology & Cell Biology, Simmons Cancer Institute, Southern Illinois University School of Medicine, 913 N. Rutledge Street, Springfield, IL 62794, USA.
Hunan University of Traditional Chinese Medicine · CNSouthern Illinois University School of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress has long been known as a pathogenic factor of ulcerative colitis (UC) and colitis-associated colorectal cancer (CAC), but the effects of secondary carbonyl lesions receive less emphasis. In inflammatory conditions, reactive oxygen species (ROS), such as superoxide anion free radical (O2 (∙-)), hydrogen peroxide (H2O2), and hydroxyl radical (HO(∙)), are produced at high levels and accumulated to cause oxidative stress (OS). In oxidative status, accumulated ROS can cause protein dysfunction and DNA damage, leading to gene mutations and cell death. Accumulated ROS could also act as chemical messengers to activate signaling pathways, such as NF-κB and p38 MAPK, to affect cell proliferation, differentiation, and apoptosis. More importantly, electrophilic carbonyl compounds produced by lipid peroxidation may function as secondary pathogenic factors, causing further protein and membrane lesions. This may in turn exaggerate oxidative stress, forming a vicious cycle. Electrophilic carbonyls could also cause DNA mutations and breaks, driving malignant progression of UC. The secondary lesions caused by carbonyl compounds may be exceptionally important in the case of host carbonyl defensive system deficit, such as aldo-keto reductase 1B10 deficiency. This review article updates the current understanding of oxidative stress and carbonyl lesions in the development and progression of UC and CAC.

Indexed as

Oxidative StressProtein CarbonylationAnimalsColitis, UlcerativeColorectal NeoplasmsDNA DamageHumansModels, Biological

Identifiers

PMID26823956
PMCPMC4707327
OpenAlexW2212591120

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.