Molecular mechanism of portal hypertensive gastropathy: an update

Abstract

Portal hypertensive gastropathy (PHG) is a serious complication and the most common gastric mucosal injury among patients afflicted with cirrhotic or non-cirrhotic portal hypertension (PHT). The pathogenesis of PHG is not completely understood and is likely to be complex. The roles of portal hypertension pressure, parenchymal liver disease, Child-Pugh classification, variceal pressure and Helicobacter pylori infection in the development of PHG are controversial. Splanchnic blood flow, the distribution of mucosal blood, vascular ectasia, local disturbances, inflammatory cell infiltration and increased cytokine production have also been examined to elucidate the underlying mechanisms of PHG. Moreover, various other elements, including prostaglandin E2 (PGE2), endothelin-1 (ET-1), tumour necrosis factor-α (TNF-α), Fas ligand (FasL)/Fas, nitric oxide (NO), oxygen free radicals and vascular endothelial growth factor (VEGF), have also been revealed to participate in the pathogenesis of PHG. This review provides an overview of the risk factors, classification and potential molecular processes involved in PHG, followed by a concise summary of our and other studies. This review aims to integrate information to deepen our understanding of the interplay between different signalling pathways involved the pathogenesis of PHG and provides insights into how these signalling pathways are regulated to control the development of PHG.