Abstract
Alternative RNA splicing is a process by which introns are removed and exons are assembled to construct different RNA transcript isoforms from a single pre-mRNA. Previous studies have demonstrated an association between dysregulation of RNA splicing and a number of clinical syndromes, but the generality to common disease has not been established. Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease affecting one-third of adults worldwide, increasing the risk of cirrhosis and hepatocellular carcinoma (HCC). In this review we focus on the change in alternative RNA splicing in fatty liver disease and the role for splicing regulation in disease progression.
Highlights
Eukaryotic protein-coding genes are usually split into exons and intervening introns that are removed by the process of RNA splicing [1]
It should be noted that all the patients in this study presented with steatosis at an early stage of Non-alcoholic fatty liver disease (NAFLD) without any evidence of NASH or cirrhosis
While RNA splicing changes have been documented in hepatocellular carcinoma (HCC) [8,9,10,11,12,13,14,15,16] and reviewed elsewhere [144,145,146], most studies in early liver disease, NAFLD or NASH, have focused on total messenger RNAs (mRNAs) changes rather than changes in individual mRNA isoforms and alternative splicing [48,49,50]
Summary
Eukaryotic protein-coding genes are usually split into exons and intervening introns that are removed by the process of RNA splicing [1]. These introns can be spliced out in the pre-mRNA at different locations and efficiencies to form different arrangements of exons in the final mRNA transcripts through the use of alternative splice sites [2] This process allows for greater RNA and protein diversity than would be predicted by the number of genes [3, 39]. Kinases and phosphatases that perform post-translational modifications of splicing factors have been identified [7, 46] These different mechanisms expand the versatility of alternative splicing, allowing the body to produce a wide variety of proteins and molecules based off of a relatively limited genome. NAFLD is strongly associated with obesity, and several obesity-linked genes have been shown to be regulated by alternative splicing [61,62,63,64]; Pihlajamaki et al
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