Discussing the role of circular RNA in the pathogenesis of non-alcoholic fatty liver disease and its complications

YEPMO, MÉLISSA; Potier, Jean-Baptiste; Pinget, M.; Grabarz, Anastasia; Bouzakri, Karim; Bourie, Aurore Dumond

doi:10.3389/fendo.2022.1035159

Cited by 4 publications

(3 citation statements)

References 97 publications

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“…Circ_0057558 promotes NAFLD by regulating ROCK1/AMPK signalling, which acts as a miR-206 sponge [21]. There are review reports that circRNAs have potential roles in the development of NAFLD and can become potential therapeutic strategies for NAFLD [22].…”

Section: Discussionmentioning

confidence: 99%

CircDock6 promotes NAFLD by regulating IGF1R through targeting mmu-let-7 g-5p

Li,

Yu,

Ding

et al. 2023

Preprint

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Circular RNAs (circRNAs) are a novel kind of noncoding RNA with a closed ring structure. An increasing number of studies have shown that it plays an important role in NAFLD. In this study, we used circDock6 to explore its role and molecular mechanism in the progression of NAFLD. qRT‒PCR was used to detect the circDock6 expression level in SD liver tissues and HFD tissues. The regulatory effects of circDock6 in NAFLD were evaluated by Oil Red “O” staining, triglyceride detection, and western blot (WB) analysis. CircDock6 was significantly upregulated in HFD liver tissues compared to SD tissues. Additionally, Oil Red “O” staining and triglyceride detection revealed that decreased expression levels of circDock6 inhibited lipid droplet formation and reduced triglyceride content. CircDock6 acts as a mmu-let-7 g-5p sponge to promote the progression of NAFLD by regulating IGF1R. Our data demonstrated that circDock6 was expressed at high levels in HFD tissues. Knockdown of circDock6 expression inhibited NAFLD progression by regulating IGF1R through targeting mmu-let-7 g-5p.

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Section: Discussionmentioning

confidence: 99%

CircDock6 promotes NAFLD by regulating IGF1R through targeting mmu-let-7 g-5p

Li,

Yu,

Ding

et al. 2023

Preprint

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“…Notably, studies on mice with CCl4-induced LF have predominantly explored the association between circRNAs and HSCs fibrogenic activation. 129 It has been demonstrated that some circRNAs contribute to HSCs activation by upregulating the expressions of the fibrogenic marker gene in response to the various pro-fibrotic signaling pathways, like TGF-β, JAK/STAT, PI3K/Akt, Hedgehog (Hh), etc. 130 CircPWWP2A increases the expression level of follistatin-like receptor 1 and Toll-like receptor 4 by suppressing miR-203 and miR-223, respectively, thereby activating the TGF-β signaling pathway.…”

Section: Circular Rnasmentioning

confidence: 99%

Mechanisms of Epigenetic Regulation in the Fibrogenic Activation of Hepatic Stellate Cells in Non-alcoholic Fatty Liver Disease

Garbuzenko

2024

Gene Expr

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Non-alcoholic fatty liver disease (NAFLD) is an extremely prevalent disease, and the presence and severity of liver fibrosis are considered one of the most important factors determining its prognosis. Hepatic stellate cells (HSCs) are essential in hepatic fibrogenesis associated with NAFLD. A number of factors underlying NAFLD pathogenesis may promote HSCs activation, leading to the development of profibrotic and proinflammatory signs. In addition, for the fibrogenic transdifferentiation of quiescent HSCs, alterations in multiple genes are necessary, where epigenetic regulation plays a defining role. Epigenetic regulation induces changes in gene activity without altering the coding sequence, and these changes are stably inherited after the factor causing the alteration has disappeared. Epigenetic modifications comprise several regulatory mechanisms, including DNA methylation, covalent histone modification, chromatin remodeling, and non-coding RNAs. Since the mechanisms underlying epigenetic regulation of HSCs fibrogenic activation are reversible and dynamic, molecular targeted therapies aimed at correcting these mechanisms provide promising prospects for novel therapeutic approaches for treating liver fibrosis

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“…They can act as microRNA sponges or regulate protein function. Altered circRNA expression profiles have been associated with NAFLD and obesity, affecting the pathways involved in insulin resistance and lipid metabolism [ 123 ]. Lastly, several lncRNAs have been found to be dysregulated in NAFLD, potentially influencing the pathways related to inflammation, lipid metabolism, and fibrosis [ 118 ].…”

Section: Noncoding Rnasmentioning

confidence: 99%

Epigenetic Regulation in Lean Nonalcoholic Fatty Liver Disease

Αγγελετοπούλου

Kalafateli

Tsounis

et al. 2023

IJMS

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Nonalcoholic fatty liver disease (NAFLD), the most prominent cause of chronic liver disease worldwide, is a rapidly growing epidemic. It consists of a wide range of liver diseases, from steatosis to nonalcoholic steatohepatitis, and predisposes patients to liver fibrosis, cirrhosis, and even hepatocellular carcinoma. NAFLD is strongly correlated with obesity; however, it has been extensively reported among lean/nonobese individuals in recent years. Although lean patients demonstrate a lower prevalence of diabetes mellitus, central obesity, dyslipidemia, hypertension, and metabolic syndrome, a percentage of these patients may develop steatohepatitis, advanced liver fibrosis, and cardiovascular disease, and have increased all-cause mortality. The pathophysiological mechanisms of lean NAFLD remain vague. Studies have reported that lean NAFLD demonstrates a close association with environmental factors, genetic predisposition, and epigenetic modifications. In this review, we aim to discuss and summarize the epigenetic mechanisms involved in lean NAFLD and to introduce the interaction between epigenetic patterns and genetic or non genetic factors. Several epigenetic mechanisms have been implicated in the regulation of lean NAFLD. These include DNA methylation, histone modifications, and noncoding-RNA-mediated gene regulation. Epigenetics is an area of special interest in the setting of lean NAFLD as it could provide new insights into the therapeutic options and noninvasive biomarkers that target this under-recognized and challenging disorder.

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Discussing the role of circular RNA in the pathogenesis of non-alcoholic fatty liver disease and its complications

Cited by 4 publications

References 97 publications

CircDock6 promotes NAFLD by regulating IGF1R through targeting mmu-let-7 g-5p

CircDock6 promotes NAFLD by regulating IGF1R through targeting mmu-let-7 g-5p

Mechanisms of Epigenetic Regulation in the Fibrogenic Activation of Hepatic Stellate Cells in Non-alcoholic Fatty Liver Disease

Epigenetic Regulation in Lean Nonalcoholic Fatty Liver Disease

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