2009
DOI: 10.1111/j.1440-1746.2009.05949.x
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Effect of miRNA‐10b in regulating cellular steatosis level by targeting PPAR‐α expression, a novel mechanism for the pathogenesis of NAFLD

Abstract: The established miRNA profile of the steatotic L02 cell model and the novel effect of miRNA-10b in regulating hepatocyte steatosis may provide a new explanation of the pathogenesis of NAFLD.

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Cited by 130 publications
(81 citation statements)
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“…Furthermore, miRNAs can also indirectly infl uence network output by targeting key network hubs, such as transcription factors ( 94 ). For example, critical lipid-sensitive transcription factors controlling hepatic metabolism, such as the LXR and PPAR families, have been shown to be functional targets of multiple miRNAs (LXR ␣ : miR-613; PPAR ␣ : miR-21, miR-10b, miR-141; PPAR ␥ : miR-23a, miR-27b, miR-130) ( 85,(94)(95)(96)(97)(98)(99). Moreover, complex feedback loops between transcription factors and miRNAs appear to control hepatocyte differentiation and possibly other aspects of liver biology (100)(101)(102).…”
mentioning
confidence: 99%
“…Furthermore, miRNAs can also indirectly infl uence network output by targeting key network hubs, such as transcription factors ( 94 ). For example, critical lipid-sensitive transcription factors controlling hepatic metabolism, such as the LXR and PPAR families, have been shown to be functional targets of multiple miRNAs (LXR ␣ : miR-613; PPAR ␣ : miR-21, miR-10b, miR-141; PPAR ␥ : miR-23a, miR-27b, miR-130) ( 85,(94)(95)(96)(97)(98)(99). Moreover, complex feedback loops between transcription factors and miRNAs appear to control hepatocyte differentiation and possibly other aspects of liver biology (100)(101)(102).…”
mentioning
confidence: 99%
“…124 MiR-10b also targets PPAR-a, which plays a major role in NAFLD pathogenesis, and may regulate steatosis in murine models of NAFLD. 125 Changes in miRs, particularly increased expression of miR-705 and -1224 and decreased expression of miR-182 and -199a have also been contributed to impaired hepatic lipid homeostasis and inflammatory cascade in alcoholic as well as nonalcoholic steatohepatitis. 116 Together these studies may provide novel diagnostic markers and therapeutic targets for NAFLD.…”
Section: Non-alcoholic Fatty Liver Disease (Nafld)mentioning
confidence: 99%
“…In addition, peroxisome proliferator-activated receptor (PPARα) is responsible for the increase in the oxidation of fatty acids and the decrease in serum levels of triglycerides. In patients with NAFLD, PPARα levels are decreased considerably but those of the prolipogenic transcription factor Sterol Regulatory Element Binding Proteins (SERBP-1c) are significantly increased [37,38]. For these reasons, PPARα is also considered to be an interesting target to study in relation to lipid metabolism and obesity.…”
Section: Therapeutic Implicationsmentioning
confidence: 99%