Effect of miRNA‐10b in regulating cellular steatosis level by targeting PPAR‐α expression, a novel mechanism for the pathogenesis of NAFLD

Zheng, Lin; Lv, Guoliang; Sheng, Jifang; Yang, Yida

doi:10.1111/j.1440-1746.2009.05949.x

Cited by 133 publications

(81 citation statements)

References 45 publications

(75 reference 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%

Complexity of microRNA function and the role of isomiRs in lipid homeostasis

Vickers

Sethupathy

Baran-Gale

et al. 2013

Journal of Lipid Research

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mentioning

confidence: 99%

Complexity of microRNA function and the role of isomiRs in lipid homeostasis

Vickers

Sethupathy

Baran-Gale

et al. 2013

Journal of Lipid Research

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“…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%

MicroRNAs in Liver Disease: Bench to Bedside

Shah

Nelson

Kowdley

2013

Journal of Clinical and Experimental Hepatology

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MicroRNAs (miRs) are small non-coding RNAs that negatively regulate gene expression by pairing with partially complementary target sequences in the 3 0 UTRs of mRNAs to promote degradation and/or block translation. Aberrant miR expression is associated with development of multiple diseases including hepatic diseases. The role of miRs in the regulation of gene expression and rapid progress in the field of microRNA research are resulting in momentum toward development of diagnostic markers and novel therapeutic strategies for human liver diseases. Recent studies provide clear evidence that miRs are abundant in the liver and modulate a diverse spectrum of biological functions, thereby supporting an association between alterations of miR homeostasis and pathological liver diseases. Here we review the role of miRs in liver as their physiological and pathological importance has been demonstrated in metabolism, immunity, viral hepatitis, oncogenesis, fatty liver diseases (alcoholic and non-alcoholic), drug-induced liver injury, fibrosis as well as acute liver failure. ( J CLIN EXP HEPATOL 2013;3:231-242)

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“…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%