Activation of NOD1 and NOD2 in the development of liver injury and cancer

Omaru, Naoya; Watanabe, Tomohiro; Kamata, Ken; Minaga, Kosuke; Kudo, Masatoshi

doi:10.3389/fimmu.2022.1004439

Cited by 9 publications

(7 citation statements)

References 59 publications

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“…Pathway enrichment study identified the activation of NOD1/NOD2 in liver tissues of the heat stress group which triggers proinflammatory and type I interferon responses, contributing to liver injury. These receptors play a role in recognizing bacterial pathogens, inducing liver inflammation, and have associations with innate immune activation in metabolic diseases, with studies suggesting that blocking NOD1 can be protective against tissue injury 61 , 62 . TREM-1 (Triggering Receptor Expressed on Myeloid Cells 1) signaling was also activated in heat-stressed liver tissues and is implicated in liver inflammation and fibrosis by promoting hepatic inflammation, activating stellate cells, and serving as a master regulator of Kupffer cell activation and linked to inflammation, lipid accumulation, fibrosis, and tumor progression in liver-related diseases 63 .…”

Section: Discussionmentioning

confidence: 99%

Periodic heat waves-induced neuronal etiology in the elderly is mediated by gut-liver-brain axis: a transcriptome profiling approach

Roy,

Saha,

Bose

et al. 2024

Sci Rep

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Heat stress exposure in intermittent heat waves and subsequent exposure during war theaters pose a clinical challenge that can lead to multi-organ dysfunction and long-term complications in the elderly. Using an aged mouse model and high-throughput sequencing, this study investigated the molecular dynamics of the liver-brain connection during heat stress exposure. Distinctive gene expression patterns induced by periodic heat stress emerged in both brain and liver tissues. An altered transcriptome profile showed heat stress-induced altered acute phase response pathways, causing neural, hepatic, and systemic inflammation and impaired synaptic plasticity. Results also demonstrated that proinflammatory molecules such as S100B, IL-17, IL-33, and neurological disease signaling pathways were upregulated, while protective pathways like aryl hydrocarbon receptor signaling were downregulated. In parallel, Rantes, IRF7, NOD1/2, TREM1, and hepatic injury signaling pathways were upregulated. Furthermore, current research identified Orosomucoid 2 (ORM2) in the liver as one of the mediators of the liver-brain axis due to heat exposure. In conclusion, the transcriptome profiling in elderly heat-stressed mice revealed a coordinated network of liver-brain axis pathways with increased hepatic ORM2 secretion, possibly due to gut inflammation and dysbiosis. The above secretion of ORM2 may impact the brain through a leaky blood–brain barrier, thus emphasizing intricate multi-organ crosstalk.

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Section: Discussionmentioning

confidence: 99%

Periodic heat waves-induced neuronal etiology in the elderly is mediated by gut-liver-brain axis: a transcriptome profiling approach

Roy,

Saha,

Bose

et al. 2024

Sci Rep

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“…For example, RNA-seq analysis suggested that Ala might also regulate the NOD-like signaling pathway. Studies have shown that a high-fat diet causes intestinal leakage and activates NOD1 and NOD2 in organs [ 39 ]. Also, the expression of both NOD1 and NOD2 was upregulated in HFD mice [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

Alantolactone attenuates high-fat diet-induced inflammation and oxidative stress in non-alcoholic fatty liver disease

Wang,

Jiang,

Jin

et al. 2024

Nutr. Diabetes

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Background Nonalcoholic fatty liver disease (NAFLD) is a chronic disease with an increasing incidence, which can further develop into liver fibrosis and hepatocellular carcinoma at the end stage. Alantolactone (Ala), a sesquiterpene lactone isolated from Asteraceae, has shown anti-inflammatory effects in different models. However, the therapeutic effect of Ala on NAFLD is not clear. Methods C57BL/6 mice were fed a high-fat diet (HFD) to induce NAFLD. After 16 weeks, Ala was administered by gavage to observe its effect on NAFLD. RNA sequencing of liver tissues was performed to investigate the mechanism. In vitro, mouse cell line AML-12 was pretreated with Ala to resist palmitic acid (PA)-induced inflammation, oxidative stress and fibrosis. Results Ala significantly inhibited inflammation, fibrosis and oxidative stress in HFD-induced mice, as well as PA-induced AML-12 cells. Mechanistic studies showed that the effect of Ala was related to the induction of Nrf2 and the inhibition of NF-κB. Taken together, these findings suggested that Ala exerted a liver protective effect on NAFLD by blocking inflammation and oxidative stress. Conclusions The study found that Ala exerted a liver protective effect on NAFLD by blocking inflammation and oxidative stress, suggesting that Ala is an effective therapy for NAFLD.

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“…The recognition of Microbe-Associated Molecular Pattern (MAMP) by NOD1 has been demonstrated to impact hepatocarcinogenesis and the development of liver damage ( 47 ). Furthermore, NOD1 has been found to upregulate the tumorigenicity of human cervical squamous cell carcinoma, thereby promoting cancer progression and metastasis ( 48 ).…”

Section: Discussionmentioning

confidence: 99%

Expression of pyroptosis-associated genes and construction of prognostic model for thyroid cancer

Guo,

Yuan,

Jiang

et al. 2023

Transl Cancer Res

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Background Thyroid cancer (THCA) is a common endocrine malignancy. This study aimed to explore the expression of pyroptosis-related genes in THCA and establish a prognosis prediction model. Methods Differentially expressed pyroptosis-related genes (DEPRGs) were identified in The Cancer Genome Atlas (TCGA) and the Molecular Signatures Database (MSigDB). Subsequently, these genes were subjected to Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. A least absolute shrinkage and selection operator (LASSO) regression model was employed to establish a DEPRG signature, and its reliability was validated through survival analysis and receiver operating characteristic (ROC) curves. Patients in TCGA-THCA cohort were stratified into two risk groups. The biological functions of the genes between the two risk groups were assessed through gene set enrichment analysis (GSEA) and gene set variation analysis (GSVA). Finally, expression of DEPRGs was validated using datasets from the Gene Expression Omnibus (GEO) and the Human Protein Atlas (HPA) databases. Results Six DEPRGs were identified in TCGA dataset. Through LASSO Cox regression analysis, we determined IL6 , TP63 , NOD1 , and BAX to be significant. Kaplan-Meier survival analysis demonstrated that patients with THCA expressing high levels of NOD1 and classified as low-risk individuals exhibited prolonged survival. The multifactorial ROC curves yielded area under the curve (AUC) scores exceeding 0.7 for risk score, age, and T-stage, affirming their significance as independent prognostic factors as determined by multivariate analysis. Additionally, we observed elevated expression levels of BAX and NOD1 in THCA using data derived from the HPA database and the GEO dataset. Conclusions We established a novel DEPRG signature for predicting the prognosis of THCA, potentially offering a promising therapeutic marker for THCA treatment.

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Activation of NOD1 and NOD2 in the development of liver injury and cancer

Cited by 9 publications

References 59 publications

Periodic heat waves-induced neuronal etiology in the elderly is mediated by gut-liver-brain axis: a transcriptome profiling approach

Periodic heat waves-induced neuronal etiology in the elderly is mediated by gut-liver-brain axis: a transcriptome profiling approach

Alantolactone attenuates high-fat diet-induced inflammation and oxidative stress in non-alcoholic fatty liver disease

Expression of pyroptosis-associated genes and construction of prognostic model for thyroid cancer

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