ArticleFrontiers in genetics2022
Profile analysis and functional modeling identify circular RNAs in nonalcoholic fatty liver disease as regulators of hepatic lipid metabolism.
Article in Frontiers in genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- CircRNAs in hepatic lipid metabolism: regulatory mechanisms and clinical implications.Frontiers in genetics · 2026Review
- Role of Circular RNAs in Liver Diseases.International journal of medical sciences · 2026Review
- Circ_KIAA0922 regulates Saos-2 cell proliferation and osteogenic differentiation by regulating the miR-148a-3p/SMAD5 axis and activating the TGF-β signaling pathway.Intractable & rare diseases research · 2023Article
- Overview of CircRNAs Roles and Mechanisms in Liver Fibrosis.Biomolecules · 2023Review
- Circular RNAs in hepatocellular carcinoma: biogenesis, function, and pathology.Frontiers in genetics · 2023Review
Corrections and comments
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Authors and funding
8 authors.
Funding
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Abstract
Nonalcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease, associated with an outcome of hepatic fibrosis/cirrhosis and hepatocellular carcinoma. However, limited exploration of the underlying mechanisms hinders its prevention and treatment. To investigate the mechanisms of epigenetic regulation in NAFLD, the expression profile of circular RNA (circRNA) of rodents in which NAFLD was induced by a high-fat, high-cholesterol (HFHC) diet was studied. Modeling of the circRNA-microRNA (miRNA) -mRNA regulatory network revealed the functional characteristics of NAFLD-specific circRNAs. The targets and effects in the liver of such NAFLD-specific circRNAs were further assessed. Our results uncovered that the downregulation of 28 annotated circRNAs characterizes HFHC diet-induced NAFLD. Among the downregulated circRNAs, long intergenic non-protein coding RNA, P53 induced transcript (LNCPINT) -derived circRNAs (circ_0001452, circ_0001453, and circ_0001454) targeted both miR-466i-3p and miR-669c-3p. Their deficiency in NAFLD abrogated the circRNA-based inhibitory effect on both miRNAs, which further inactivated the AMPK signaling pathway
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