The Oxidative Damage and Inflammation Mechanisms in GERD-Induced Barrett's Esophagus

Deqiang Han; Chao Zhang

doi:10.3389/fcell.2022.885537

The Oxidative Damage and Inflammation Mechanisms in GERD-Induced Barrett's Esophagus

Front Cell Dev Biol. 2022 May 26:10:885537. doi: 10.3389/fcell.2022.885537. eCollection 2022.

Authors

Deqiang Han^{1

2}, Chao Zhang¹

Affiliations

¹ Department of General Surgery, National Clinical Research Center for Geriatric Diseases, Xuanwu Hospital of Capital Medical University, Beijing, China.
² Cell Therapy Center, Beijing Institute of Geriatrics, Xuanwu Hospital Capital Medical University, National Clinical Research Center for Geriatric Diseases, Beijing, China.

Abstract

Barrett's esophagus is a major complication of gastro-esophageal reflux disease and an important precursor lesion for the development of Barrett's metaplasia and esophageal adenocarcinoma. However, the cellular and molecular mechanisms of Barrett's metaplasia remain unclear. Inflammation-associated oxidative DNA damage could contribute to Barrett's esophagus. It has been demonstrated that poly(ADP-ribose) polymerases (PARPs)-associated with ADP-ribosylation plays an important role in DNA damage and inflammatory response. A previous study indicated that there is inflammatory infiltration and oxidative DNA damage in the lower esophagus due to acid/bile reflux, and gastric acid could induce DNA damage in culture esophageal cells. This review will discuss the mechanisms of Barrett's metaplasia and adenocarcinoma underlying oxidative DNA damage in gastro-esophageal reflux disease patients based on recent clinical and basic findings.

Keywords: Barrett’s esophagus; DNA damage; NF-kappa B; polyADP-ribose polymerase 1; transdifferentiation.

Publication types

Review