Published online Aug 26, 2022. doi: 10.12998/wjcc.v10.i24.8436
Peer-review started: April 1, 2022
First decision: June 7, 2022
Revised: June 16, 2022
Accepted: July 16, 2022
Article in press: July 16, 2022
Published online: August 26, 2022
Processing time: 136 Days and 13 Hours
Although gastroesophageal reflux disease (GERD), a common chronic disease in clinical practice, has been widely studied, its potential adverse impact on patients is still a significant clinical concern. It is necessary to understand the pathogenesis of the disease and choose appropriate treatment according to its mechanism. The pathogenesis of GERD is diverse and complex. As the traditional treatment methods are expensive and ineffective in alleviating symptoms in some patients, new treatment options need to be explored. Our previous study suggested that the activation of nuclear factor-kappa beta (NF-κB) in esophageal mucosa may be related to the injury of epithelial barrier function caused by reflux. Based on the literature and our previous study results, it is speculated that inhibition of NF-κB activation may block the insult of GERD on the esophageal mucosal barrier. NF-κB may play an important role in the development of GERD. This article reviews the pathogenesis of GERD and the relationship between NF-κB and GERD, in order to provide new strategies for the treatment of GERD.
Core Tip: Gastroesophageal reflux disease (GERD) is one of the most common chronic diseases. Current treatments, including drugs and surgery, have significant side effects and some patients do not respond to treatment. This article reviews the pathogenesis of GERD, especially the relationship between the NF-κB pathway and GERD. We also assessed the latest studies on the effects of drugs inhibiting the NF-κB pathway in GERD, providing new possibilities for the treatment of GERD.
