Abstract
Proteolysis is an irreversible post-translational modification that regulates protein function and signal transduction. This includes remodelling of the extracellular matrix, release of membrane-bound cytokines and receptor ectodomains, as well as the initiation of intracellular signalling cues. Members of the adamalysin protease subfamily, in particular the ADAM (a disintegrin and metalloprotease) and ADAMTS (the ADAM containing thrombospondin motif) families, are involved in these processes. This review presents an overview of how ADAM and ADAMTS proteins are involved in liver physiology and pathophysiology.
Highlights
The liver harbours different cell types, including hepatocytes, cholangiocytes, resident macrophages called Kupffer cells (KCs), sinusoidal endothelial cells (SECs) and hepatic stellate cells (HSCs)
Reports using in vitro experiments demonstrated that ADAM17 mediates the release of EGFR ligands in hepatocytes upon exposure to tumour necrosis factor (TNF) α [51] or TGFβ [52], suggesting that ADAM17 on hepatocytes might be involved in liver regeneration (Table 1)
As summarised above, selected members of ADAM and ADAMTS proteinase families display altered expression in different liver pathologies, and a mechanistical role in the pathology has been shown for some members
Summary
The liver harbours different cell types, including hepatocytes, cholangiocytes, resident macrophages called Kupffer cells (KCs), sinusoidal endothelial cells (SECs) and hepatic stellate cells (HSCs). Members of the metzincin Journal of Renal and Hepatic Disorders 2019; 3(1): 23–32 protease family have been shown to be involved in different aspects of chronic liver disease and tumour formation. The catalytic domain is conserved among the ADAM family members and contains the zinc-binding motif (HExGHxxGxxHD) (Figure 1 a and b) [17].
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