The Potential Role of Cellular Senescence in Non-Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) represents an increasing global health burden. Cellular senescence develops in response to cellular injury, leading not only to cell cycle arrest but also to alterations of the cellular phenotype and metabolic functions. In this review, we critically discuss the currently existing evidence for the involvement of cellular senescence in NAFLD in order to identify areas requiring further exploration. Hepatocyte senescence can be a central pathomechanism as it may foster intracellular fat accumulation, fibrosis and inflammation, also due to secretion of senescence-associated inflammatory mediators. However, in some non-parenchymal liver cell types, such as hepatic stellate cells, senescence may be beneficial by reducing the extracellular matrix deposition and thereby reducing fibrosis. Deciphering the detailed interaction between NAFLD and cellular senescence will be essential to discover novel therapeutic targets halting disease progression.

Automated summary

Cellular senescence plays a significant role in non-alcoholic fatty liver disease (NAFLD), but further research is needed to understand the specific mechanisms. Hepatocyte senescence may contribute to fat accumulation, fibrosis, and inflammation, while senescence in non-parenchymal liver cells could potentially reduce fibrosis. A comprehensive understanding of the interaction between NAFLD and cellular senescence is crucial for identifying novel therapeutic targets.