Silencing lncRNA NEAT1 reduces nonalcoholic fatty liver fat deposition by regulating the miR-139-5p/c-Jun/SREBP-1c pathway

Jin, Sisi; Cui, Lin; Xin, Lin; Zheng, Juzeng; Guan, Huaqin

doi:10.1016/j.aohep.2021.100584

Cited by 17 publications

(16 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additionally, a study demonstrated that upregulation of PPARG can accelerate the progression of adipogenic hepatic steatosis 41 . In the NAFLD cellular sample, the expression of JUN was considerably elevated, suggesting that miR-139-5p overexpression is an indirect approach to dampen the JUN expression level 42 . An animal test suggested that epidermal growth factor receptor (EGFR) activation exacerbates the severity of NAFLD due to dysfunction of lipid metabolism 43 .…”

Section: Discussionmentioning

confidence: 96%

The identification of metabolites from gut microbiota in NAFLD via network pharmacology

Gupta

Min

et al. 2023

Sci Rep

View full text Add to dashboard Cite

The metabolites of gut microbiota show favorable therapeutic effects on nonalcoholic fatty liver disease (NAFLD), but the active metabolites and mechanisms against NAFLD have not been documented. The aim of the study was to investigate the active metabolites and mechanisms of gut microbiota against NAFLD by network pharmacology. We obtained a total of 208 metabolites from the gutMgene database and retrieved 1256 targets from similarity ensemble approach (SEA) and 947 targets from the SwissTargetPrediction (STP) database. In the SEA and STP databases, we identified 668 overlapping targets and obtained 237 targets for NAFLD. Thirty-eight targets were identified out of those 237 and 223 targets retrieved from the gutMgene database, and were considered the final NAFLD targets of metabolites from the microbiome. The results of molecular docking tests suggest that, of the 38 targets, mitogen-activated protein kinase 8-compound K and glycogen synthase kinase-3 beta-myricetin complexes might inhibit the Wnt signaling pathway. The microbiota-signaling pathways-targets-metabolites network analysis reveals that Firmicutes, Fusobacteria, the Toll-like receptor signaling pathway, mitogen-activated protein kinase 1, and phenylacetylglutamine are notable components of NAFLD and therefore to understanding its processes and possible therapeutic approaches. The key components and potential mechanisms of metabolites from gut microbiota against NAFLD were explored utilizing network pharmacology analyses. This study provides scientific evidence to support the therapeutic efficacy of metabolites for NAFLD and suggests holistic insights on which to base further research.

show abstract

Section: Discussionmentioning

confidence: 96%

The identification of metabolites from gut microbiota in NAFLD via network pharmacology

Gupta

Min

et al. 2023

Sci Rep

View full text Add to dashboard Cite

show abstract

“…In the present review, NEAT1 expression levels were found to be upregulated in serum and PBMCs of NAFLD patients, and it was also upregulated in both NAFLD-related inflammation and advanced fibrosis, which was consistent with previous studies conducted in vitro and in vivo. Recent preclinical studies have revealed that NEAT1 is abundant in the liver and is a risk factor affecting NAFLD, which could promote the NAFLD progress by facilitating hepatic lipid accumulation [ 60 , 61 , 62 ]. We first summarized NEAT1 expression levels in NAFLD patients, and they showed good diagnostic performance.…”

Section: Discussionmentioning

confidence: 99%

LncRNA and circRNA in Patients with Non-Alcoholic Fatty Liver Disease: A Systematic Review

Zeng

Liu

et al. 2023

Biomolecules

View full text Add to dashboard Cite

Non-alcoholic fatty liver disease (NAFLD) is currently the most common cause of chronic liver disease worldwide. Early identification and prompt treatment are critical to optimize patient management and improve long-term prognosis. Long non-coding RNA (lncRNA) and circular RNA (circRNA) are recently emerging non-coding RNAs, and are highly stable and easily detected in the circulation, representing a promising non-invasive approach for predicting NAFLD. A literature search of the Pubmed, Embase, Web of Science, and Cochrane Library databases was performed and 36 eligible studies were retrieved, including 18 on NAFLD, 13 on nonalcoholic steatohepatitis (NASH), and 11 on fibrosis and/or cirrhosis. Dynamic changes in lncRNA expression were associated with the occurrence and progression of NAFLD, among which lncRNA NEAT1, MEG3, and MALAT1 exhibited great potential as biomarkers for NAFLD. Moreover, mitochondria-located circRNA SCAR can drive metaflammation and its inhibition might be a promising therapeutic target for NASH. In this systematic review, we highlight the great potential of lncRNA/circRNA for early diagnosis and progression assessment of NAFLD. To further verify their clinical value, large-cohort studies incorporating lncRNA and circRNA expression both in liver tissue and blood should be conducted. Additionally, detailed studies on the functional mechanisms of NEAT1, MEG3, and MALAT1 will be essential for elucidating their roles in diagnosing and treating NAFLD, NASH, and fibrosis.

show abstract

“…Additionally, a study demonstrated that upregulation of PPARG can accelerate the progression of adipogenic hepatic steatosis [39]. In the NAFLD cellular sample, the expression of JUN was considerably elevated, suggesting that miR-139-5p overexpression is an indirect approach to dampen the JUN expression level [40]. An animal test suggested that epidermal growth factor receptor (EGFR) activation exacerbates the severity of NAFLD due to dysfunction of lipid metabolism [41].…”

Section: Discussionmentioning

confidence: 99%

Exploration of metabolites from gut microbiota against nonalcoholic fatty liver disease: A network pharmacology-based study

Gupta

Min

et al. 2022

Preprint

View full text Add to dashboard Cite

Background: The metabolites of gut microbiota show favorable therapeutic effects on nonalcoholic fatty liver disease (NAFLD), but the active metabolites and mechanisms against NAFLD have not been documented. The aim of the study was to investigate the active metabolites and mechanisms of gut microbiota against NAFLD by network pharmacology. Results: We obtained a total of 208 metabolites from the gutMgene database and retrieved 1,256 targets from similarity ensemble approach (SEA) and 947 targets from the SwissTargetPrediction (STP) database. In the SEA and STP databases, we identified 668 overlapping targets and obtained 237 targets for NAFLD. Thirty-eight targets were identified out of those 237 and 223 targets retrieved from the gutMgene database, and were considered the final NAFLD targets of metabolites from the microbiome. The results of molecular docking tests suggest that, of the 38 targets, mitogen-activated protein kinase 8-compound K and glycogen synthase kinase-3 beta-myricetin complexes might inhibit the Wnt signaling pathway. The microbiota-signaling pathways-targets-metabolites network analysis reveals that Firmicutes, Fusobacteria, the Toll-like receptor signaling pathway, mitogen-activated protein kinase 1, and phenylacetylglutamine are notable components of NAFLD.Conclusion: The key components and potential mechanisms of metabolites from gut microbiota against NAFLD were explored utilizing network pharmacology analyses. This study provides scientific evidence to support the therapeutic efficacy of metabolites for NAFLD and suggests holistic insights for further research.

show abstract

Silencing lncRNA NEAT1 reduces nonalcoholic fatty liver fat deposition by regulating the miR-139-5p/c-Jun/SREBP-1c pathway

Cited by 17 publications

References 28 publications

The identification of metabolites from gut microbiota in NAFLD via network pharmacology

The identification of metabolites from gut microbiota in NAFLD via network pharmacology

LncRNA and circRNA in Patients with Non-Alcoholic Fatty Liver Disease: A Systematic Review

Exploration of metabolites from gut microbiota against nonalcoholic fatty liver disease: A network pharmacology-based study

Contact Info

Product

Resources

About