Abstract
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.
Highlights
This fact, which is against the known paradigm of cellular senescence as a driver of Non-alcoholic fatty liver disease (NAFLD), highlights the complex mechanisms and effects cellular senescence may have in advanced disease stages, where multiple cell types, including stellate cells as the major ECM producers, are involved [48] (Table 1)
Telomere length in leukocytes shortened in patients with diabetes type 2 who developed NAFLD
NAFLD and degree of fibrosis was associated with shorter telomeres, cellular senescence (p21) and DNA
Summary
A recently published trial in 1339 biopsy-proven NAFLD patients indicated that non-obese or lean patients with NAFLD have a similar liver-related and overall mortality compared with obese NAFLD patients [10]. Targeting NAFLD with the aim to prevent disease progression may be an incremental component of patient management strategies. Further disease progression is characterized by inflammation and without cirrhosis bears the risk of developing hepatocellular carcinoma (HCC). There is evidence showing that are cellular senescence, especially in Cellular senescence a term describing cells which in cell cycle arrest but remain hepatocytes, may modulate fat accumulation and inflammation in patients with different metabolically active [21]. Modulate fat accumulation and inflammation patients with different role of of cellular senescence in NAFLDthis and its effect intercellular crosstalk as a central stages [21,22]. Role ofof cellular in NAFLD and its effect on intercellular crosstalk as a central driver of disease progression
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