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In addition, experimental studies have shown that the elevation of GSH can inhibit the activation of hepatic stellate cells [33], which is a key driving factor for extracellular matrix deposition and fibrosis, thereby preventing the progression of liver fibrosis [34]
Upon cell internalization via endocytosis mechanisms, these nanoparticles disrupt endosomal membranes through the proton sponge effect, facilitating the intracellular delivery of exogenous nucleic acids
The aim of this review is to update and discuss the hepatic diseases associated with ABC transporter mutations, the genetic and environmental effects that influence the severity of disease, typical presentations of these cholestatic hepatic diseases, diagnostic considerations, and treatment options
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