Recent insights into contributing factors in the pathogenesis of cirrhotic ascites

Abstract

Cirrhotic ascites refers to the accumulation of fluid in the peritoneal cavity due to severe liver disease and impaired liver function, which leads to poor blood circulation in the body, increased pressure in the hepatic sinus wall, and the exudation of fluid from the plasma into the peritoneal cavity. Cirrhotic ascites is a common complication of cirrhosis and poses a threat to the health and lives of modern people, causing a heavy social burden worldwide. So far, there are no effective treatment methods available to improve the quality and quantity of life for patients and their partners; existing drugs can only alleviate the symptoms of cirrhotic ascites and slow down its progression. This article aims to carefully examine the pathogenesis of cirrhotic ascites by exploring various contributing factors such as portal hypertension, renal dysfunction, inflammation, growth factors, oxidative stress, immunocytes, and gut microbiota. The purpose is to gain better insights and deeper understanding of the mechanisms involved in this condition.

Keywords: cirrhotic ascites; growth factors; immunocytes; inflammation; oxidative stress; portal hypertension; renal dysfunction.

FIGURE 1

The pathophysiology of cirrhotic ascites. (By Figdraw). Under the stimulation of various factors, the stable state of the liver cell environment is disrupted, leading to the development of cirrhosis and the occurrence of ascites. These factors include portal hypertension, renal dysfunction, inflammation, growth factors, oxidative stress, immunocytes, and gut microbiota. These changes ultimately result in alterations in the normal structure and function of the liver, leading to the development of cirrhotic ascites. HSC, hepatic stellate cell; RAAS, renin - angiotensin - aldosterone system; HRS, hepatorenal syndrome; ROS, reactive oxygen species; OS, oxidative stress; TGF-β, transforming growth factor-beta; HGF, hepatocyte growth factor; VEGF, vascular endothelial growth factor; MET, epithelial transition factor; TNF-α, tumor necrosis factor-α; IL, interleukin.

FIGURE 2

The pathogenesis of gut microbiota in the development of cirrhotic ascites. (By Figdraw). The pathogenesis of gut microbiota in the development of cirrhotic ascites involves the imbalance of intestinal microbiota, leading to impairment of the intestinal mucosal barrier and reduced intestinal barrier function. This imbalance further promotes the translocation of bacteria and toxins. These bacteria and toxins activate immune, inflammatory responses, and oxidative stress, ultimately resulting in liver dysfunction and the formation of ascites. TNF-α, tumor necrosis factor-α; IL, interleukin; HDACs, histone deacetylases; AC, adenylate cyclase; OS, oxidative stress; SCFAs, short-chain fatty acids; LPS, lipopolysaccharides.