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Background <p>Alcohol 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.</p> Results <p>It was found that &lt; 0.5% alcohol or a &lt; 30-minute exposure benefited cell growth primarily through autophagy, while &gt; 0.5% alcohol or a &gt; 30-minute exposure caused cell death, including apoptosis, necroptosis, and ferroptosis, but not pyroptosis. Autophagy took place within the first 30&#xa0;min of alcohol exposure, followed by apoptosis, which peaked at 2&#xa0;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.</p> Conclusions <p>Low 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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月9日

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

摘要

Background

Alcohol 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.

Results

It 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.

Conclusions

Low 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.