FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3117005106> ?p ?o ?g. }

• W3117005106 endingPage "1882" @default.
• W3117005106 startingPage "1881" @default.
• W3117005106 abstract "I read the recent article by Chai et al1Chai C. et al.Gastroenterology. 2020; 159: 999-1014Abstract Full Text Full Text PDF PubMed Scopus (16) Google Scholar with great interest. The authors have shown that the beneficial role of increased hepatic miR-122 induced by an RAR-related orphan receptor A (RORA) agonist in the improvement of hepatic lipotoxicity, liver fibrosis, and body weight in nonalcoholic steatohepatitis (NASH) was mediated through the activation of RORA to reveal not only local but also remote action for alleviating NASH progression.1Chai C. et al.Gastroenterology. 2020; 159: 999-1014Abstract Full Text Full Text PDF PubMed Scopus (16) Google Scholar However, the linkage between miR-122 and metabolic modulation remains incompletely clear. The activation of RORA was implicated in metabolic circadian rhythm, and the dietary composition of free fatty acids connected with RORA–hepatic miR-122–triglyceride circuitry seemed crucial. According to my previous commentary on miR-122 in hepatic lipid metabolism, the effect of hepatic miR-122 on metabolic shift can be altered under different nutritional conditions.2Chung H.H. Gastroenterology. 2018; 154: 1552-1553Abstract Full Text Full Text PDF PubMed Scopus (3) Google Scholar In early stage NASH, the compensated mechanism is consistent with the findings by Chia et al because hepatic miR-122 levels in the high-fat diet group were lower than those in the normal diet group, whereas circulating and white adipose tissues (WAT) miR-122 levels were higher in high-fat diet group than those in normal diet group. Furthermore, silencing endogenous hepatic miR-122 by antagomiR-122 was accompanied by decreased circulating and WAT miR-122 levels, indicating decreased hepatic miR-122 secretion to circulation and peripheral tissues in late-stage NASH abolished the compensated mechanism and enhanced lipid accumulation. Similarly, circulating miR-122 levels tended to diminish before nonalcoholic fatty liver disease (NAFLD) progression to fibrosis stage in a patient with long-term follow-up,3Akuta N. et al.Hepatol Int. 2016; 10: 647-656Crossref PubMed Scopus (25) Google Scholar suggesting that the variation of circulating miR-122 could serve as the prognostic indicator for hepatocarcinogenesis. In the abstract, it seems the term “increased insulin resistance” should be revised to “increased insulin sensitivity” based on the authors’ findings. Hepatic miR-122 associated with remote tissues reflected systemic communication for the regulation of energy metabolism. MiR-122 has been considered as the biomarker for the prediction of metabolic syndrome and type-2 diabetes, and circulating miR-122 levels were decreased after treatment with atorvastatin, indicating the clinical application in the evaluation of metabolic abnormalities.4Willeit P. et al.Diabetes. 2017; 66: 347-357Crossref PubMed Scopus (131) Google Scholar In addition, NASH-induced hepatic lipotoxicity, elevated circulating miR-122 levels were closely associated with insulin resistance.5Wang R. et al.Eur J Endocrinol. 2015; 172: 291-300Crossref PubMed Scopus (92) Google Scholar Additionally, the gluconeogenesis involved in hepatic glucose metabolism and glucose transporter 4 dysfunction in glucose uptake of skeletal muscle related to insulin resistance should be considered for miR-122 inhibition.6Sendi H. et al.PLoS One. 2018; 13e0200847Crossref PubMed Scopus (27) Google Scholar In the present report by Chai et al, increased hepatic miR-122 attenuated insulin resistance in insulin tolerance test, but hepatic miR-122 on gluconeogenesis, glucose uptake, pancreatic β cell function and insulin signaling originated from NASH was not well-investigated. Although the modulation of miR-122 exhibited beneficial effects on WAT inflammation, circulating miR-122 levels were negatively correlated with brown adipose tissues activity linked to thermoregulation in healthy humans.7Okamatsu-Ogura Y. et al.Sci Rep. 2019; 9: 13243Crossref PubMed Scopus (12) Google Scholar Moreover, adipokines secreted from adipose tissues initiated a series of signal transduction in metabolic regulation, but how miR-122 interacts with adipokines remains unknown. Leptin promoted hepatic fibrosis mimicking obese patients with hyperleptinaemia linked to leptin resistance through the suppression of miR-122 activity.8Cao Q. et al.Toxicol Appl Pharmacol. 2018; 339: 143-150Crossref PubMed Scopus (12) Google Scholar Thus, the role of hepatic miR-122 in brown adipose tissue and mitochondrial functions has not been completely mentioned, and the effects of miR-122 on adipokines require more investigations to verify. Notably, the induction of miR-122 by specific activators ameliorated NAFLD progression by anti-inflammation and antifibrosis, which can be applied to other metabolic disorders and carcinogenesis. Taken together, the pharmacologic mechanisms of identified compounds via the modulation of endogenous miR-122 provide a promising direction in energy metabolism, but the interaction with other critical miRNAs, metabolic hormones and target gene profiling is still under further investigation. Agonist of RORA Attenuates Nonalcoholic Fatty Liver Progression in Mice via Up-regulation of MicroRNA 122GastroenterologyVol. 159Issue 3PreviewDevelopment of nonalcoholic steatohepatitis (NASH) is associated with reductions in hepatic microRNA122 (MIR122); the RAR related orphan receptor A (RORA) promotes expression of MIR122. Increasing expression of RORA in livers of mice increases expression of MIR122 and reduces lipotoxicity. We investigated the effects of a RORA agonist in mouse models of NASH. Full-Text PDF ReplyGastroenterologyVol. 160Issue 5PreviewIn response to our recent publication in your journal,1 Hsien-Hui Chung wanted us to focus on the linkage between miR-122 and metabolic modulation, including interaction with other critical miRNAs, metabolic hormones and target gene profiling. In response to the comments, we would like to emphasize that our article is focused on the effect of the new RORα agonist (RS-2982) on miR-122 regulation, and its beneficial therapeutic effect on nonalcoholic steatohepatitis (NASH). This report was an additional observation that was added to our hypothesis, that microRNAs have hormonal like effects. Full-Text PDF" @default.
• W3117005106 created "2021-01-05" @default.
• W3117005106 creator A5077027927 @default.
• W3117005106 date "2021-04-01" @default.
• W3117005106 modified "2023-10-16" @default.
• W3117005106 title "The Noticeable Crosslink between miR-122 and Metabolic Dysfunction" @default.
• W3117005106 cites W1989146491 @default.
• W3117005106 cites W2340023004 @default.
• W3117005106 cites W2557910380 @default.
• W3117005106 cites W2772612206 @default.
• W3117005106 cites W2793197374 @default.
• W3117005106 cites W2883298821 @default.
• W3117005106 cites W2972332478 @default.
• W3117005106 cites W3026716048 @default.
• W3117005106 doi "https://doi.org/10.1053/j.gastro.2020.12.054" @default.
• W3117005106 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33387526" @default.
• W3117005106 hasPublicationYear "2021" @default.
• W3117005106 type Work @default.
• W3117005106 sameAs 3117005106 @default.
• W3117005106 citedByCount "0" @default.
• W3117005106 crossrefType "journal-article" @default.
• W3117005106 hasAuthorship W3117005106A5077027927 @default.
• W3117005106 hasBestOaLocation W31170051061 @default.
• W3117005106 hasConcept C126322002 @default.
• W3117005106 hasConcept C134018914 @default.
• W3117005106 hasConcept C185592680 @default.
• W3117005106 hasConcept C2777391703 @default.
• W3117005106 hasConcept C2778163477 @default.
• W3117005106 hasConcept C2778772119 @default.
• W3117005106 hasConcept C2778913445 @default.
• W3117005106 hasConcept C2779134260 @default.
• W3117005106 hasConcept C2779478299 @default.
• W3117005106 hasConcept C44353895 @default.
• W3117005106 hasConcept C511355011 @default.
• W3117005106 hasConcept C71924100 @default.
• W3117005106 hasConceptScore W3117005106C126322002 @default.
• W3117005106 hasConceptScore W3117005106C134018914 @default.
• W3117005106 hasConceptScore W3117005106C185592680 @default.
• W3117005106 hasConceptScore W3117005106C2777391703 @default.
• W3117005106 hasConceptScore W3117005106C2778163477 @default.
• W3117005106 hasConceptScore W3117005106C2778772119 @default.
• W3117005106 hasConceptScore W3117005106C2778913445 @default.
• W3117005106 hasConceptScore W3117005106C2779134260 @default.
• W3117005106 hasConceptScore W3117005106C2779478299 @default.
• W3117005106 hasConceptScore W3117005106C44353895 @default.
• W3117005106 hasConceptScore W3117005106C511355011 @default.
• W3117005106 hasConceptScore W3117005106C71924100 @default.
• W3117005106 hasIssue "5" @default.
• W3117005106 hasLocation W31170051061 @default.
• W3117005106 hasOpenAccess W3117005106 @default.
• W3117005106 hasPrimaryLocation W31170051061 @default.
• W3117005106 hasRelatedWork W2035484352 @default.
• W3117005106 hasRelatedWork W2048104183 @default.
• W3117005106 hasRelatedWork W2068269311 @default.
• W3117005106 hasRelatedWork W2110966479 @default.
• W3117005106 hasRelatedWork W2140792307 @default.
• W3117005106 hasRelatedWork W2259778815 @default.
• W3117005106 hasRelatedWork W2748952813 @default.
• W3117005106 hasRelatedWork W2890749350 @default.
• W3117005106 hasRelatedWork W2995497694 @default.
• W3117005106 hasRelatedWork W3030938700 @default.
• W3117005106 hasVolume "160" @default.
• W3117005106 isParatext "false" @default.
• W3117005106 isRetracted "false" @default.
• W3117005106 magId "3117005106" @default.
• W3117005106 workType "article" @default.