Hypertension, TLR4 activation in brain and cardiac hypertrophy

Mehta, Jawahar L.; Ding, Zufeng; Liu, Shijie; Wang, Xianwei; Khaidakov, Magomed

doi:10.1093/cvr/cvu128

Cited by 12 publications

(10 citation statements)

References 13 publications

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“…CD274 [175] [190], PDGFC (platelet derived growth factor C) [191], TLR2 [192], PRKAB2 [193], HDAC9 [194], NCOA4 [195], LATS2 [196], DICER1 [197], IL1RN [198], GCH1 [148], EGR1 [199] IQGAP2 [351], GCLC (glutamate-cysteine ligase catalytic subunit) [352], VEGFA (vascular endothelial growth factor A) [353], ITGB1 [354], LDLR (low density lipoprotein receptor) [355], TLR6 [316], SIRT1 [356], FGL2 [357], TET2 [358], PHF2 [328], VEGFB (vascular endothelial growth factor B) [359], SELENOM (selenoprotein M) [360], TRPM4 [361], OLFM2 [362] and ATAD3A [363] are thought to be involved in non-alcoholic fatty liver disease. Altered expression of ATOH8 [364], STAT1 [365], ARG1 [366], TLR4 [367], VNN1 [368], ABCA1 [369], IFIH1 [370], PTGS2 [371], F2RL1 [289], CYP2D6 [372], PDK4 [373], RNF213 [374], JAK2 [375], NOTCH2 [376], PDGFC (platelet derived growth factor C) [377], TLR2 [378], CYP1B1 [379], IL1RN [380], GCH1…”

Section: Construction Of the Tf-hub Gene Regulatory Networkmentioning

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: Construction Of the Tf-hub Gene Regulatory Networkmentioning

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

View full text Add to dashboard Cite

show abstract

“…More importantly, TLR4/NF-κB is closely associated with the regulation of blood pressure. Studies have shown that subcutaneous infusion of angiotensin II (Ang II) increases the levels of TLR4 in an Ang II-induced hypertensive rat model, thereby inducing myocardial inflammation and increasing cardiac sympathetic nerve activity; elevated blood pressure subsequently increases cardiac afterload and hinders left ventricular contraction, thereby eventually leading to ventricular hypertrophy [90,91]. Blocking TLR4/NF-κB in the brain in a spontaneously hypertensive rat model significantly decreases blood pressure [92].…”

Section: Cardiac Hypertrophymentioning

confidence: 99%

Inappropriate Activation of TLR4/NF-κB is a Cause of Heart Failure

Zhou

Lin

et al. 2022

CVIA

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Significance: Heart failure, a disease with extremely high incidence, is closely associated with inflammation and oxidative stress. The Toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) pathway plays an important role in the occurrence and development of heart failure. Recent advances: Previous studies have shown that TLR4/NF-κB causes heart failure by inducing oxidative stress and inflammation; damaging the endothelia; promoting fibrosis; and inducing myocardial hypertrophy, apoptosis, pyroptosis, and autophagy. Critical issues: Understanding the pathogenesis of heart failure is essential for the treatment of this disease. In this review, we outline the mechanisms underlying TLR4/NF-κB pathway-mediated heart failure and discuss drugs that alleviate heart failure by regulating the TLR4/NF-κB pathway. Future directions: During TLR4/NF-κB overactivation, interventions targeting specific receptor antagonists may effectively alleviate heart failure, thus providing a basis for the development of new anti-heart failure drugs.

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“…Similarly, continuous subcutaneous infusion of Ang II increased the level of brain TLR4 in the Ang II-induced hypertensive rat model, activated myocardial inflammation and increased sympathetic activity, both of which are responsible for hypertension and cardiac hypertrophy. Conversely, central blockade of TLR4 reportedly reduced mean arterial blood pressure, suppressed production of pro-inflammatory mediators, and eventually attenuated cardiac hypertrophy (25,26). Recently, blockade of TLR4 was found to display less hypertrophy in isoproterenol (ISO)-induced cardiac hypertrophy in rats (27).…”

Section: Tlr4 Initiates Inflammatory Response In Cardiac Hypertrophymentioning

confidence: 99%

Key Player in Cardiac Hypertrophy, Emphasizing the Role of Toll-Like Receptor 4

Zheng

Kong

Yang

et al. 2020

Front. Cardiovasc. Med.

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Toll-like receptor 4 (TLR4), a key pattern recognition receptor, initiates the innate immune response and leads to chronic and acute inflammation. In the past decades, accumulating evidence has implicated TLR4-mediated inflammatory response in regulation of myocardium hypertrophic remodeling, indicating that regulation of the TLR4 signaling pathway may be an effective strategy for managing cardiac hypertrophy's pathophysiology. Given TLR4's significance, it is imperative to review the molecular mechanisms and roles underlying TLR4 signaling in cardiac hypertrophy. Here, we comprehensively review the current knowledge of TLR4-mediated inflammatory response and its interaction ligands and co-receptors, as well as activation of various intracellular signaling. We also describe the associated roles in promoting immune cell infiltration and inflammatory mediator secretion, that ultimately cause cardiac hypertrophy. Finally, we provide examples of some of the most promising drugs and new technologies that have the potential to attenuate TLR4-mediated inflammatory response and prevent or reverse the ominous cardiac hypertrophy outcomes.

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Hypertension, TLR4 activation in brain and cardiac hypertrophy

Cited by 12 publications

References 13 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

Inappropriate Activation of TLR4/NF-κB is a Cause of Heart Failure

Key Player in Cardiac Hypertrophy, Emphasizing the Role of Toll-Like Receptor 4

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