4.6 Review

Inflammatory mediators in gastroesophageal reflux disease: impact on esophageal motility, fibrosis, and carcinogenesis

出版社

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpgi.00454.2009

关键词

cytokines; motility; stricture; stenosis

资金

  1. Deutsche Forschungsgemeinschaft, Germany
  2. Crohn's and Colitis Foundation of America
  3. National Institutes of Health, Bethesda, MD
  4. Astra Zeneca
  5. Takeda
  6. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK057030] Funding Source: NIH RePORTER

向作者/读者索取更多资源

Rieder F, Biancani P, Harnett K, Yerian L, Falk GW. Inflammatory mediators in gastroesophageal reflux disease: impact on esophageal motility, fibrosis, and carcinogenesis. Am J Physiol Gastrointest Liver Physiol 298: G571-G581, 2010. First published March 18, 2010; doi: 10.1152/ajpgi.00454.2009.-Gastroesophageal reflux disease (GERD) is one of the most common problems in clinical practice today. It is widely believed that functional and structural abnormalities of the gastroesophageal junction as well as an abnormal exposure to gastroduodenal contents are the main contributors to its pathogenesis. Novel findings of the inflammatory process in GERD suggest a far more complex process involving multifaceted inflammatory mechanisms. This review summarizes knowledge about the expression of inflammatory mediators in GERD and their potential cellular sources and provides an integrated concept of disease pathogenesis. In addition we evaluate the contribution of inflammatory mediators to well-known complications of GERD, namely motility abnormalities, fibrosis, and carcinogenesis. Novel findings regarding the pathophysiology of esophageal inflammation should enhance our understanding of GERD and its complications and provide new treatment insights.

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