Evidence map›Paper›PMID 41957693›Full record

ArticleBMC molecular and cell biology2026

Alcohol exposure induces ferroptosis-dominated programmed cell death in esophageal epithelial cells.

Dongxue Wang, Zhenyu Jiang, Zhiyi Meng, Wei Hou, Tong Dang, Xianmei Meng, Jianyuan Chai

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC molecular and cell biology, 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

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

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

7 authors.

Dongxue Wang *Inner Mongolia Institute of Digestive Diseases, The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, 30 Hudemulin Rd, Baotou, 014030, China.
Zhenyu Jiang *Inner Mongolia Institute of Digestive Diseases, The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, 30 Hudemulin Rd, Baotou, 014030, China.
Zhiyi MengInner Mongolia Institute of Digestive Diseases, The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, 30 Hudemulin Rd, Baotou, 014030, China.
Wei HouInner Mongolia Institute of Digestive Diseases, The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, 30 Hudemulin Rd, Baotou, 014030, China.
Tong DangInner Mongolia Institute of Digestive Diseases, The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, 30 Hudemulin Rd, Baotou, 014030, China.
Xianmei MengInner Mongolia Institute of Digestive Diseases, The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, 30 Hudemulin Rd, Baotou, 014030, China. mxm_2fy@163.com.
Jianyuan ChaiInner Mongolia Institute of Digestive Diseases, The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, 30 Hudemulin Rd, Baotou, 014030, China. Jianyuan.chai@gmail.com.

Funding

the National Natural Science Foundation of China 81960445the Science and Technology Program of the Joint Fund of Scientific Research for the Public Hospitals of Inner Mongolia Academy of Medical Sciences 2023GLLH212
6 · The paper itself

Abstract

backgroundAlcohol consumption has been a risk factor for nearly 200 diseases. Although swallowing an alcoholic beverage takes only a few seconds, the substance can stick to the esophageal lining longer after drinking. What alcohol does to the esophageal cells is not fully understood. This study explored the issue through in vitro experimentation.

resultsIt was found that < 0.5% alcohol or a < 30-minute exposure benefited cell growth primarily through autophagy, while > 0.5% alcohol or a > 30-minute exposure caused cell death, including apoptosis, necroptosis, and ferroptosis, but not pyroptosis. Autophagy took place within the first 30 min of alcohol exposure, followed by apoptosis, which peaked at 2 h, and then was gradually replaced by necroptosis as the alcohol exposure continued. Ferroptosis initiated immediately after contact with alcohol and became dominant progressively. However, as alcohol exposure continued, cells developed tolerance through anastasis, reviving and reforming the epithelial monolayer.

conclusionsLow concentrations of alcohol or a short exposure promote esophageal cell growth owing to autophagy, while higher concentrations or a longer exposure cause multiple forms of cell death, including apoptosis, necroptosis, and ferroptosis. Yet, cells can recover from alcohol insult through anastasis as the exposure extends.

Indexed as

ApoptosisEpithelial CellsEsophagusEthanolFerroptosisAutophagyCell LineCell ProliferationHumansNecroptosisEthanolAlcoholAnastasisApoptosisAutophagyEsophageal cellFerroptosisNecroptosisPyroptosis

Identifiers

PMID41957693
PMCPMC13173723

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.