Anti-Angiogenic Effects of Natural Compounds in Diet-Associated Hepatic Inflammation

Nutrients. 2023 Jun 14;15(12):2748. doi: 10.3390/nu15122748.

Abstract

Alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD) are the most common causes of chronic liver disease and are increasingly emerging as a global health problem. Such disorders can lead to liver damage, resulting in the release of pro-inflammatory cytokines and the activation of infiltrating immune cells. These are some of the common features of ALD progression in ASH (alcoholic steatohepatitis) and NAFLD to NASH (non-alcoholic steatohepatitis). Hepatic steatosis, followed by fibrosis, lead to a continuous progression accompanied by angiogenesis. This process creates hypoxia, which activates vascular factors, initiating pathological angiogenesis and further fibrosis. This forms a vicious cycle of ongoing damage and progression. This condition further exacerbates liver injury and may contribute to the development of comorbidities, such as metabolic syndrome as well as hepatocellular carcinoma. Increasing evidence suggests that anti-angiogenic therapy may have beneficial effects on these hepatic disorders and their exacerbation. Therefore, there is a great interest to deepen the knowledge of the molecular mechanisms of natural anti-angiogenic products that could both prevent and control liver diseases. In this review, we focus on the role of major natural anti-angiogenic compounds against steatohepatitis and determine their potential therapeutic benefits in the treatment of liver inflammation caused by an imbalanced diet.

Keywords: ALD; ASH; NAFLD; NASH; angiogenesis; hepatocellular carcinoma; inflammation; liver disease; natural compounds; steatosis.

Publication types

  • Review

MeSH terms

  • Diet, High-Fat
  • Fibrosis
  • Humans
  • Inflammation / metabolism
  • Liver / metabolism
  • Liver Diseases, Alcoholic* / metabolism
  • Liver Neoplasms* / metabolism
  • Non-alcoholic Fatty Liver Disease* / complications
  • Non-alcoholic Fatty Liver Disease* / etiology

Grants and funding

This research received no external funding.