Administration of isoliquiritigenin prevents nonalcoholic fatty liver disease through a novel <scp>IQGAP2‐CREB‐SIRT1</scp> axis

Zhang, Li; Yang, Shengye; Qi-Li, Feng-Rong; Liu, Xiao-Xiao; Zhang, Weitao; Peng, Chao; Wu, Ping; Li, Ping; Li, Pingping; Xu, Xiaojun

doi:10.1002/ptr.7101

Cited by 22 publications

(12 citation statements)

References 69 publications

(98 reference statements)

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“…Altered expression of CEACAM1 [176], ACSL1 [285], STAT1 [286], TLR4 [287], ABCA1 [288], TLR5 [183], F2RL1 [289], CYP2D6 [290], PDK4 [291], RNF213 [186], JAK2 [292], TLR8 [189], NOTCH2 [293], CENPJ (centromere protein J) [294], FNIP1 [295], TLR2 [296], KIDINS220 [297], DUSP6 [298], CYP1B1 [299], S1PR3 [300], NCOA2 [301], HDAC9 [302], PELI1 [303], EGR1 [304], HIF1A [305], CCR2 [306], IRAK3 [307], KLF3 [308], VEGFA (vascular endothelial growth factor A) [309], OGT (O-linked N-acetylglucosamine (GlcNAc) transferase) [310], PHLPP1 [213], FMR1 [311], IGF2R [312], PRKAR1A [313], WDR11 [314], LDLR (low density lipoprotein receptor) [315], TLR6 [316], SIRT1 [317], ALDH1A1 [318], NOD2 [319], ACSL4 [320], ELOVL6 [321], VCAN (versican) [322], CLIC5 [323], CLCN3 [324], OSBPL11 [162], HELZ2 [325], TET2 [326], KDM6A [327], PHF2 [328], PHGDH (phosphoglycerate dehydrogenase) [329], VEGFB (vascular endothelial growth factor B) [330], ZBTB7A [331], PC (pyruvate carboxylase) [332], CCR7 [333], PRDX2 [334], MAF1 [335], HSPB1 [336], ESF1 [281], LGALS3 [337], OLFM2 [338] and HDAC11 [339] had been confirmed in obesity. CEACAM1 [340], ACSL1 [341], TLR4 [342], ABCA1 [343], TLR5 [344], CYP2D6 [345], JAK2 [346], NOTCH2 [347], DDX3X [348], NCOA4 [349], EGR1 [350], IQGAP2 [351], GCLC (glut...…”

Section: Discussionmentioning

confidence: 99%

Identification of novel prognostic targets in coronary artery disease and related complications using bioinformatics and next generation sequencing data analysis

Vastrad¹,

Vastrad²

2023

Preprint

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Coronary artery disease (CAD) is the most common cardiovascular disorder and the leading cause of heart related deaths in world. Increasing molecular targets have been discovered for CAD and CAD - related complications prognosis and therapy. However, there is still an urgent need to identify novel biomarkers. Therefore, we evaluated biomarkers that might help the diagnosis and treatment of CAD and CAD related complications. We searched next generation sequencing (NGS) dataset (GSE202625) and identified differentially expressed genes (DEGs) by comparing CAD and normal control samples using DESeq2. Gene ontology (GO) and pathway enrichment analyses of the DEGs were performed using the g:Profiler online database. The protein protein interaction (PPI) network was plotted with IMEx interactome and visualized using Cytoscape. Module analysis of the PPI network was done using PEWCC1. MiRNA hub gene regulatory network and TF hub gene regulatory network analysis was performed to identify the hub genes, miRNAs and TFs. Receiver operating characteristic (ROC) curve analysis was used to predict the diagnostic effectiveness of the hub genes. A total of 118 DEGs (479 up regulated genes and 479 down regulated genes) were detected. The GO enrichment analysis indicated that the DEGs most significantly enriched in cellular response to stimulus and biosynthetic process. The REACTOME pathway enrichment analysis revealed that the DEGs were most significantly enriched in immune system and eukaryotic translation elongation. PPI network, modules, miRNA hub gene regulatory network and TF hub gene regulatory network analysis demonstrated that EGR1, SIRT1, STAT1, LRRK2, HIF1A, CSNK2B, RPS3, RPS2, RPS4X and HDAC11 were the hub genes. On the whole, the findings of this study enhance our understanding of the potential molecular mechanisms of CAD and CAD-related complications, and provide potential targets for further research.

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Section: Discussionmentioning

confidence: 99%

Identification of novel prognostic targets in coronary artery disease and related complications using bioinformatics and next generation sequencing data analysis

Vastrad¹,

Vastrad²

2023

Preprint

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“…Limited proteolysis combined with mass spectrometry (LiP‐SMap) was done according to a former report 23,24 . Briefly, adipocyte lysates from three independent biological replicates were aliquoted in equivalent volumes containing 100 μg of proteome sample and incubated for 10 min at 25°C with vehicle or TA (final concentration: 33 nmol).…”

Section: Methodsmentioning

confidence: 99%

“…Limited proteolysis combined with mass spectrometry (LiP-SMap) was done according to a former report. 23,24 Briefly, adipocyte lysates from three independent biological replicates were aliquoted in equivalent volumes containing 100 μg of proteome sample and incubated for 10 min at 25°C with vehicle or TA (final concentration: 33 nmol). Proteinase K from Tritirachium album (Sigma Aldrich) was added simultaneously to all the proteome-TA samples at a proteinase K to substrate mass ratio of 1:100 and incubated at 25°C for 5 min.…”

Section: Limited Proteolysis Combined With Mass Spectrometrymentioning

confidence: 99%

Traumatic acid inhibits ACSL4 associated lipid accumulation in adipocytes to attenuate high‐fat diet‐induced obesity

Gao,

Zhang,

Dong

et al. 2023

The FASEB Journal

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Obesity is a major health concern that lacks effective intervention strategies. Traumatic acid (TA) is a potent wound‐healing agent in plants, considered an antioxidant food ingredient. This study demonstrated that TA treatment significantly reduced lipid accumulation in human adipocytes and prevented high‐fat diet induced obesity in zebrafish. Transcriptome sequencing revealed TA‐activated fatty acid (FA) degradation and FA metabolism signaling pathways. Moreover, western blotting and quantitative polymerase chain reaction showed that TA inhibited the expression of long‐chain acyl‐CoA synthetase‐4 (ACSL4). Overexpression of ACSL4 resulted in the reversal of TA beneficiary effects, indicating that the attenuated lipid accumulation of TA was regulated by ACSL4 expression. Limited proteolysis‐mass spectrometry and microscale thermophoresis were then used to confirm hexokinase 2 (HK2) as a direct molecular target of TA. Thus, we demonstrated the molecular basis of TA in regulating lipid accumulation and gave the first evidence that TA may function through the HK2‐ACSL4 axis.

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“…Hence, SIRT1 activity is required to activate the transcription of PPARα target genes including FGF21 in the liver [ 86 ]. Moreover, it has been reported that natural compounds and drugs used for the treatment of NAFLD targeting the PPARα signaling pathway are dependent on SIRT1 activity [ 87 , 88 , 89 ]. Moreover, in both adipocytes and hepatocytes, it has been shown that the depletion of SIRT1 reduces the expression of several PPARα target genes related to lipid metabolism and mitochondrial biogenesis [ 90 , 91 ].…”

Section: Epigenetic Interaction Partners In Crime In Pparα-dependent ...mentioning

confidence: 99%

PPARα in the Epigenetic Driver Seat of NAFLD: New Therapeutic Opportunities for Epigenetic Drugs?

et al. 2022

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Nonalcoholic fatty liver disease (NAFLD) is a growing epidemic and the most common cause of chronic liver disease worldwide. It consists of a spectrum of liver disorders ranging from simple steatosis to NASH which predisposes patients to further fibrosis, cirrhosis and even hepatocarcinoma. Despite much research, an approved treatment is still lacking. Finding new therapeutic targets has therefore been a main priority. Known as a main regulator of the lipid metabolism and highly expressed in the liver, the nuclear receptor peroxisome proliferator-activated receptor-α (PPARα) has been identified as an attractive therapeutic target. Since its expression is silenced by DNA hypermethylation in NAFLD patients, many research strategies have aimed to restore the expression of PPARα and its target genes involved in lipid metabolism. Although previously tested PPARα agonists did not ameliorate the disease, current research has shown that PPARα also interacts and regulates epigenetic DNMT1, JMJD3, TET and SIRT1 enzymes. Moreover, there is a growing body of evidence suggesting the orchestrating role of epigenetics in the development and progression of NAFLD. Therefore, current therapeutic strategies are shifting more towards epigenetic drugs. This review provides a concise overview of the epigenetic regulation of NAFLD with a focus on PPARα regulation and highlights recently identified epigenetic interaction partners of PPARα.

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Administration of isoliquiritigenin prevents nonalcoholic fatty liver disease through a novel IQGAP2‐CREB‐SIRT1 axis

Cited by 22 publications

References 69 publications

Identification of novel prognostic targets in coronary artery disease and related complications using bioinformatics and next generation sequencing data analysis

Identification of novel prognostic targets in coronary artery disease and related complications using bioinformatics and next generation sequencing data analysis

Traumatic acid inhibits ACSL4 associated lipid accumulation in adipocytes to attenuate high‐fat diet‐induced obesity

PPARα in the Epigenetic Driver Seat of NAFLD: New Therapeutic Opportunities for Epigenetic Drugs?

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