scholarly journals Shared Molecular Mechanisms between Atherosclerosis and Periodontitis by Analyzing the Transcriptomic Alterations of Peripheral Blood Monocytes

2021 ◽  
Vol 2021 ◽  
pp. 1-28
Author(s):  
Wanchen Ning ◽  
Yihong Ma ◽  
Simin Li ◽  
Xin Wang ◽  
Hongying Pan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Platelet Activation ◽  
Molecular Mechanisms ◽  
Gene Interaction ◽  
Mapk Signaling ◽  
Functional Enrichment ◽  
Venn Diagram ◽  
Bacterial Invasion ◽  
The Core

Objective. This study investigated the nature of shared transcriptomic alterations in PBMs from periodontitis and atherosclerosis to unravel molecular mechanisms underpinning their association. Methods. Gene expression data from PBMs from patients with periodontitis and those with atherosclerosis were each downloaded from the GEO database. Differentially expressed genes (DEGs) in periodontitis and atherosclerosis were identified through differential gene expression analysis. The disease-related known genes related to periodontitis and atherosclerosis each were downloaded from the DisGeNET database. A Venn diagram was constructed to identify crosstalk genes from four categories: DEGs expressed in periodontitis, periodontitis-related known genes, DEGs expressed in atherosclerosis, and atherosclerosis-related known genes. A weighted gene coexpression network analysis (WGCNA) was performed to identify significant coexpression modules, and then, coexpressed gene interaction networks belonging to each significant module were constructed to identify the core crosstalk genes. Results. Functional enrichment analysis of significant modules obtained by WGCNA analysis showed that several pathways might play the critical crosstalk role in linking both diseases, including bacterial invasion of epithelial cells, platelet activation, and Mitogen-Activated Protein Kinases (MAPK) signaling. By constructing the gene interaction network of significant modules, the core crosstalk genes in each module were identified and included: for GSE23746 dataset, RASGRP2 in the blue module and VAMP7 and SNX3 in the green module, as well as HMGB1 and SUMO1 in the turquoise module were identified; for GSE61490 dataset, SEC61G, PSMB2, SELPLG, and FIBP in the turquoise module were identified. Conclusion. Exploration of available transcriptomic datasets revealed core crosstalk genes (RASGRP2, VAMP7, SNX3, HMGB1, SUMO1, SEC61G, PSMB2, SELPLG, and FIBP) and significant pathways (bacterial invasion of epithelial cells, platelet activation, and MAPK signaling) as top candidate molecular linkage mechanisms between atherosclerosis and periodontitis.

scholarly journals Detoxification and Immune Transcriptomic Response of the Gill Tissue of Bay Scallop (Argopecten irradians) Following Exposure to the Algicide Palmitoleic Acid

Biomolecules ◽  
2018 ◽  
Vol 8 (4) ◽  
pp. 139 ◽  
Author(s):  
Cheng Chi ◽  
Sib Giri ◽  
Jin Jun ◽  
Hyoun Kim ◽  
Sang Kim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cytochrome P450 ◽  
Palmitoleic Acid ◽  
Molecular Mechanisms ◽  
Functional Enrichment ◽  
Alexandrium Tamarense ◽  
Read Length ◽  
Related Factor ◽  
Transcriptomic Response ◽  
Bay Scallop

Palmitoleic acid (PA) is an effective algicide against Alexandrium tamarense. However, the toxicological mechanism of PA exposure is unclear. The transcript abundance and differentially expressed genes (DEGs) in gills of bay scallop were investigated following 80 mg/L PA exposure up to 48 h using the Illumina HiSeq 4000 deep-sequencing platform with the recommended read length of 100 bp. De novo assembly of paired-end reads yielded 62,099 unigenes; 5414 genes were identified as being significantly increased, and 4452 were decreased. Based on gene ontology classification and enrichment analysis, the ‘cellular process’, ‘metabolic process’, ‘response to stimulus’, and ‘catalytic process’ with particularly high functional enrichment were revealed. The DEGs, which are related to detoxification and immune responses, revealed that acid phosphatase, fibrinogen C domain-containing protein, cyclic AMP-responsive element-binding protein, glutathione reductase, ATP-binding cassette, nuclear factor erythroid 2-related factor, NADPH2:quinone reductase, and cytochrome P450 4F22, 4B1, and 2C8-related gene expression decreased. In contrast, some genes related to glutathione S-transferase, C-type lectin, superoxide dismutase, toll-like receptors, and cytochrome P450 2C14, 2U1, 3A24 and 4A2 increased. The results of current research will be a valuable resource for the investigation of gene expression stimulated by PA, and will help understanding of the molecular mechanisms underlying the scallops’ response to PA exposure.

Identification of Four Key Biomarkers and Small Molecule Drugs Innasopharyngeal Carcinoma by Weighted Gene Co-expression Network Analysis

2020 ◽  
Author(s):  
Xi Pan ◽  
Jian-Hao Liu
Keyword(s):  
Gene Expression ◽  
Network Analysis ◽  
Small Molecule ◽  
Molecular Mechanisms ◽  
Enrichment Analysis ◽  
Tumor Stage ◽  
Functional Enrichment ◽  
Hub Genes ◽  
Therapeutic Goals ◽  
Small Molecule Drugs

Abstract Background Nasopharyngeal carcinoma (NPC) is a heterogeneous carcinoma that the underlying molecular mechanisms involved in the tumor initiation, progression, and migration are largely unclear. The purpose of the present study was to identify key biomarkers and small-molecule drugs for NPC screening, diagnosis, and therapy via gene expression profile analysis. Methods Raw microarray data of NPC were retrieved from the Gene Expression Omnibus (GEO) database and analyzed to screen out the potential differentially expressed genes (DEGs). The key modules associated with histology grade and tumor stage was identified by using weighted correlation network analysis (WGCNA). Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of genes in the key module were performed to identify potential mechanisms. Candidate hub genes were obtained, which based on the criteria of module membership (MM) and high connectivity. Then we used receiver operating characteristic (ROC) curve to evaluate the diagnostic value of hub genes. The Connectivity map database was further used to screen out small-molecule drugs of hub genes. Results A total of 430 DEGs were identified based on two GEO datasets. The green gene module was considered as key module for the tumor stage of NPC via WGCNA analysis. The results of functional enrichment analysis revealed that genes in the green module were enriched in regulation of cell cycle, p53 signaling pathway, cell part morphogenesis. Furthermore, four DEGs-related hub genes in the green module were considered as the final hub genes. Then ROC revealed that the final four hub genes presented with high areas under the curve, suggesting these hub genes may be diagnostic biomarkers for NPC. Meanwhile, we screened out several small-molecule drugs that have provided potentially therapeutic goals for NPC. Conclusions Our research identified four potential prognostic biomarkers and several candidate small-molecule drugs for NPC, which may contribute to the new insights for NPC therapy.

Berberine inhibits lipopolysaccharide-induced expression of inflammatory cytokines by suppressing TLR4-mediated NF-ĸB and MAPK signaling pathways in rumen epithelial cells of Holstein calves

2019 ◽  
Vol 86 (2) ◽  
pp. 171-176 ◽  
Author(s):  
Chenxu Zhao ◽  
Yazhou Wang ◽  
Xue Yuan ◽  
Guoquan Sun ◽  
Bingyu Shen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Signaling Pathways ◽  
Inflammatory Cytokines ◽  
Molecular Mechanisms ◽  
Mapk Signaling ◽  
Dependent Manner ◽  
Inflammatory Drug ◽  
Anti Inflammatory ◽  
Mapk Signaling Pathways ◽  
Rumen Epithelial Cells

AbstractSubacute ruminal acidosis (SARA) can increase the level of inflammation and induce rumenitis in dairy cows. Berberine (BBR) is the major active component of Rhizoma Coptidis, which is a type of Chinese anti-inflammatory drug for gastrointestinal diseases. The purpose of this study was to investigate the anti-inflammatory effects of BBR on lipopolysaccharide (LPS)-stimulated rumen epithelial cells (REC) and the underlying molecular mechanisms. REC were cultured and stimulated with LPS in the presence or absence of different concentrations of BBR. The results showed that cell viability was not affected by BBR. Moreover, BBR markedly decreased the concentrations and mRNA expression of pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin-1β, and interleukin-6 in the LPS-treated REC in a dose-dependent manner. Importantly, Western blotting analysis showed that BBR significantly suppressed the protein expression of toll-like receptor 4 (TLR4) and myeloid differentiation primary response protein (MyD88) and the phosphorylation of nuclear factor-κB (NF-κB), inhibitory kappa B (IκBα), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK) in LPS-treated REC. Furthermore, the results of immunocytofluorescence showed that BBR significantly inhibited the nuclear translocation of NF-κB p65 induced by LPS treatment. In conclusion, the protective effects of BBR on LPS-induced inflammatory responses in REC may be due to its ability to suppress the TLR4-mediated NF-κB and MAPK signaling pathways. These findings suggest that BBR can be used as an anti-inflammatory drug to treat inflammation induced by SARA.

scholarly journals Specific Inhibition of Interferon Signal Transduction Pathways by Adenoviral Infection

2001 ◽  
Vol 276 (50) ◽  
pp. 47136-47142 ◽  
Author(s):  
Theresa D. Joseph ◽  
Dwight C. Look
Keyword(s):  
Gene Expression ◽  
Signal Transduction ◽  
Transcription Factor ◽  
Epithelial Cells ◽  
Molecular Mechanisms ◽  
Airway Epithelial Cells ◽  
Signal Transducer ◽  
Airway Epithelial ◽  
Complex Assembly ◽  
Ifn Γ

Adenoviral evolution has generated strategies to resist host cell antiviral systems, but molecular mechanisms for evasion of interferon (IFN) effects by adenoviruses during late-phase infection are poorly defined. In this study, we examined adenovirus type 5 (AdV) effects on IFN-γ-dependent gene expression and Janus family kinase-signal transducer and activator of transcription signaling components in human tracheobronchial epithelial cells. We found that AdV infection specifically inhibited IFN-γ-dependent gene expression in airway epithelial cells without evidence of epithelial cell injury or generation of a soluble extracellular inhibitor. Furthermore, infection with AdV for 18–24 h blocked phosphorylation/activation of the Stat1 transcription factor that regulates IFN-γ-dependent genes. Although AdV also inhibited IFN-α-dependent phosphorylation of Stat1 and Stat2, interleukin-4-dependent phosphorylation of the related transcription factor Stat6 was not affected, indicating that the virus selectively affected specific signaling pathways. Our results indicate that AdV inhibition of the IFN-γ signal transduction cascade occurs through loss of ligand-induced receptor complex assembly and consequent component phosphorylation and suggest that lack of complex assembly is due to decreased expression of the IFN-γR2 chain of the IFN-γ receptor. IFN-γR2 is required at an early step in Janus family kinase-signal transducer and activator of transcription pathway activation and is expressed at low levels in airway epithelial cells, supporting the concept that adenoviral down-regulation of the level of this IFN-γ receptor component allows for persistent modulation of IFN-γ-dependent gene expression.

scholarly journals Analysis of potential genetic biomarkers and molecular mechanism of smoking-related postmenopausal osteoporosis using weighted gene co-expression network analysis and machine learning

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0257343
Author(s):  
Shaoshuo Li ◽  
Baixing Chen ◽  
Hao Chen ◽  
Zhen Hua ◽  
Yang Shao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Machine Learning ◽  
Network Analysis ◽  
Postmenopausal Osteoporosis ◽  
Molecular Mechanism ◽  
Molecular Mechanisms ◽  
Functional Enrichment ◽  
Support Vector ◽  
Hub Genes ◽  
Genetic Biomarkers

Objectives Smoking is a significant independent risk factor for postmenopausal osteoporosis, leading to genome variations in postmenopausal smokers. This study investigates potential biomarkers and molecular mechanisms of smoking-related postmenopausal osteoporosis (SRPO). Materials and methods The GSE13850 microarray dataset was downloaded from Gene Expression Omnibus (GEO). Gene modules associated with SRPO were identified using weighted gene co-expression network analysis (WGCNA), protein-protein interaction (PPI) analysis, and pathway and functional enrichment analyses. Feature genes were selected using two machine learning methods: support vector machine-recursive feature elimination (SVM-RFE) and random forest (RF). The diagnostic efficiency of the selected genes was assessed by gene expression analysis and receiver operating characteristic curve. Results Eight highly conserved modules were detected in the WGCNA network, and the genes in the module that was strongly correlated with SRPO were used for constructing the PPI network. A total of 113 hub genes were identified in the core network using topological network analysis. Enrichment analysis results showed that hub genes were closely associated with the regulation of RNA transcription and translation, ATPase activity, and immune-related signaling. Six genes (HNRNPC, PFDN2, PSMC5, RPS16, TCEB2, and UBE2V2) were selected as genetic biomarkers for SRPO by integrating the feature selection of SVM-RFE and RF. Conclusion The present study identified potential genetic biomarkers and provided a novel insight into the underlying molecular mechanism of SRPO.

scholarly journals Identify Molecular Mechanisms of Jiangzhi Decoction on Nonalcoholic Fatty Liver Disease by Network Pharmacology Analysis and Experimental Validation

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Lei Wang ◽  
Yin Zhi ◽  
Ying Ye ◽  
Miao Zhang ◽  
Xing Ma ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver Disease ◽  
Molecular Mechanisms ◽  
Enrichment Analysis ◽  
Functional Enrichment Analysis ◽  
Functional Enrichment ◽  
Active Ingredients ◽  
Nonalcoholic Fatty Liver ◽  
The Core

Background. Jiangzhi Decoction (JZD), a traditional herb mixture, has shown significant clinical efficacy against nonalcoholic fatty liver disease (NAFLD). However, its multicomponent and multitarget characteristics bring difficulty in deciphering its pharmacological mechanisms. Our study is aimed at identifying the core molecular mechanisms of JZD against NAFLD. Methods. The active ingredients were searched from Traditional Chinese Medicine Systems Pharmacology (TCMSP) database and Traditional Chinese Medicine Integrated Database (TCMID). The targets of those ingredients were identified using ChemMapper database based on 3D structure similarity. NAFLD-related genes were searched from DisGeNET database and Gene Expression Omnibus (GEO) database. Then, we performed protein-protein interaction (PPI) analysis, functional enrichment analysis, and constructed pathway networks of “herbs-active ingredients-candidate targets” and identified the core molecular mechanisms and key active ingredients in the network. Also, molecular docking was carried out to predict the ligands of candidate targets using SwissDock. Finally, the human hepatic L02 cell line was used to establish the NAFLD model in vitro. The effect and key molecules were validated by Oil Red O staining, biochemical assays, and quantitative real-time PCR (qRT-PCR). Results. We found 147 active ingredients in JZD, 1285 targets of active ingredients, 401 NAFLD-related genes, and 59 overlapped candidate targets of JZD against NAFLD. 22 core targets were obtained by PPI analysis. Finally, nuclear receptor transcription and lipid metabolism regulation were found as the core molecular mechanisms of JZD against NAFLD by functional enrichment analysis. The candidate targets PPARα and LXRα were both docked with hyperin as the most favorable interaction, and HNF4α was docked with linolenic acid ethyl ester. According to in vitro experiments, it was found that JZD had an inhibitory effect on lipid accumulation and regulatory effects on cholesterol and triglycerides. Compared with OA group, the mRNA expression levels of PPARα and HNF4α were significantly upregulated in JZD group ( P < 0.05 ), and LXRα was significantly downregulated ( P < 0.001 ). Conclusion. JZD might alleviate hepatocyte steatosis by regulating some key molecules related to nuclear receptor transcription and lipid metabolism, such as PPARα, LXRα, and HNF4α. Our study will provide the scientific evidences of the clinical efficacy of JZD against NAFLD.

scholarly journals Characteristic Features of the Transcriptome in a Rat Strain with Audiogenic Epilepsy

2022 ◽  
Author(s):  
Lyubov N. Chuvakova ◽  
Sergey Yu. Funikov ◽  
Artem I. Davletshin ◽  
Irina B. Fedotova ◽  
Mikhail B. Evgen'ev ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Repair ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Mapk Signaling ◽  
Repair System ◽  
Audiogenic Epilepsy ◽  
Rat Strain ◽  
Characteristic Features

Audiogenic epilepsy (AE), developing in rodent strains in response to sound, is widely used as the model of generalized convulsive epilepsy, while the molecular mechanisms determining AE are currently poorly understood. The brain region that is crucial for AE development isthe inferior and superior colliculi (IC, SC). We compared IC-SC gene expression profiles in rats with different AE susceptibility using transcriptome analysis.The transcriptomes were obtained from the IC-SC of Wistar rats (with no AE), Krushinsky-Molodkina (KM) strain rats (100% AE susceptible), and ”0” strain rats (with no AE) selected from F2 KM x Wistar hybrids for AE absence. KM gene expression displayed characteristic differences inboth of the strains that were not susceptible to AE. There was increased expression of a number of genes responsible for positive regulation of the MAPK signaling cascade, as well as of genes responsible for the production of interferon and several other cytokines. An increase in the expression levels of theTTR gene was found in KM rats, as well as significantly lower expression of the Msh3 gene (involved in post-replicative DNA repair systems). AE was also describedin the 101/HY mouse strain with a mutation in the locus controlling DNA repair. The DNA repair system defects could be the primary factor leading to the accumulation of mutations, which, in turn, promote AE. Keywords: udiogenic seizure, KM strain, transcriptome, TTR gene, Msh3 gene, DNA repair

scholarly journals Network Pharmacology Identifies the Mechanisms of Sang-Xing-Zhi-Ke-Fang against Pharyngitis

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Yinhe Deng ◽  
Quanjiang Li ◽  
Menglin Li ◽  
Tiantian Han ◽  
Guixian Li ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Influenza A ◽  
Molecular Mechanisms ◽  
Mapk Signaling ◽  
Venn Diagram ◽  
Network Pharmacology ◽  
Pathway Enrichment Analysis ◽  
Ras Signaling ◽  
Clinical Effects ◽  
Overlapping Genes

Background. Sang-Xing-Zhi-Ke-Fang (SXZKF) demonstrates good therapeutic effect against pharyngitis. Nevertheless, the pharmacological mechanism underlying its effectiveness is still unclear. Objective. To investigate the underlying mechanisms of SXZKF against pharyngitis using network pharmacology method. Methods. Bioactive ingredients of SXZKF were collected and screened using published literature and two public databases. Using four public databases, the overlapping genes between these bioactive compound-related and pharyngitis-related genes were identified by Venn diagram. Protein-protein interaction (PPI) was obtained using “Search Tool for the Retrieval of Interacting Genes (STRING)” database. “Database for Annotation, Visualization, and Integrated Discovery ver. 6.8 (DAVID 6.8)” was used to perform Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis to explore the molecular mechanisms of SXZKF against pharyngitis. Finally, Cytoscape 3.7.2 software was used to construct and visualize the networks. Result. A total of 102 bioactive compounds were identified. Among them, 886 compounds-related and 6258 pharyngitis-related genes were identified, including 387 overlapping genes. Sixty-three core targets were obtained, including ALB, PPARγ, MAPK3, EGF, and PTGS2. Signaling pathways closely related to mechanisms of SXZKF for pharyngitis were identified, including serotonergic synapse, VEGF signaling pathway, Fc epsilon RI signaling pathway, Ras signaling pathway, MAPK signaling pathway, and influenza A. Conclusion. This is the first identification of in-depth study of SXZKF against pharyngitis using network pharmacology. This new evidence could be informative in providing new support on the clinical effects of SXZKF on pharyngitis and for the development of personalized medicine for pharyngitis.

Identification of Potential Biomarkers in Synovial Tissue of Rheumatoid Arthritis via Integrated Microarray Analysis. Identification of Biomarkers of Rheumatoid Arthritis

2021 ◽  
Author(s):  
Li Tao ◽  
ChaoLiang Xiong ◽  
Li Xue
Keyword(s):  
Rheumatoid Arthritis ◽  
Gene Expression ◽  
Pathway Analysis ◽  
Expression Profiles ◽  
Diagnostic Value ◽  
Functional Enrichment ◽  
Venn Diagram ◽  
Ppi Network ◽  
Hub Genes ◽  
Gene Markers

Abstract Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovitis and subsequent destruction of cartilage and bone. This study aimed to explore RA-related gene markers and the underlying molecular mechanism.Material and Methods: The expression profiles of GSE77298, GSE55235 and GSE12021 were obtained from the Gene Expression Omnibus database. Then, the differential gene expression analysis was conducted between GSE77298 and GSE55235 datasets. Limma package and a Venn diagram were utilized to screen the overlapping differentially expressed genes (DEGs), and Functional enrichment and pathway analysis were performed by using DAVID database. Subsequently, a protein-protein interaction (PPI) network was established, and candidate hub genes were recognized by using STRING and Cytoscape software. Finally, another dataset (GSE12021) was used for the validation of diagnostic value of the candidate hub genes and to identify real hub genes by using receiver operating characteristic (ROC) curves.Results: A total of 385 DEGs were detected, which include 19 downregulated genes and 366 upregulated genes. GO and KEGG pathway analysis showed that DEGs was mainly enriched in various immune and inflammatory response-related functions and pathways. The PPI network was composed of 374 nodes and 767 edges. A total of 8 real hub genes (HLA-DRA, HLA-DRB1, LCK, VAV1, HLA-DPA1, HLA-DPB1, C3AR1 and CD3D) which displayed an excellent diagnostic value for RA were identified.Conclusion: these findings may provide novel and reliable biomarkers for RA, which have some interesting implications for early diagnosis, prognosis and targeted therapy.

Validation of novel hub genes and molecular mechanisms in acute lung injury using an integrative bioinformatics approach

2021 ◽  
Author(s):  
Qingchun Liang ◽  
Qin Zhou ◽  
Jinhe Li ◽  
Zhugui Chen ◽  
Zhihao Zhang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Molecular Mechanisms ◽  
Molecular Biomarkers ◽  
Functional Enrichment ◽  
Lung Injury Score ◽  
Control Group ◽  
High Morbidity ◽  
Hub Genes

Abstract Acute lung injury (ALI) is an inflammatory pulmonary disease that can easily develop into serious acute respiratory distress syndrome, which has high morbidity and mortality. However, the molecular mechanism of ALI remains unclear, and few molecular biomarkers for diagnosis and treatment have been identified. In this study, we aimed to identify novel molecular biomarkers using a bioinformatics approach. Gene expression data were obtained from the Gene Expression Omnibus database, co-expressed differentially expressed genes (CoDEGs) were identified using R software, and further functional enrichment analyses were conducted using the online tool Database for Annotation, Visualization, and Integrated Discovery. A protein–protein interaction network was established using the STRING database and Cytoscape software. Lipopolysaccharide (LPS)-induced ALI mouse model was constructed and verified. The hub genes were screened and validated in vivo. The transcription factors (TFs) and miRNAs associated with the hub genes were predicted using the NetworkAnalyst database. In total, 71 CoDEGs were screened and found to be mainly involved in the cytokine–cytokine receptor interactions, and the tumor necrosis factor and malaria signaling pathways. Animal experiments showed that the lung injury score, bronchoalveolar lavage fluid protein concentration, and wet-to-dry weight ratio were higher in the LPS group than those in the control group. Real-time polymerase chain reaction analysis indicated that most of the hub genes such as colony-stimulating factor 2 (Csf2) were overexpressed in the LPS group. A total of 20 TFs including nuclear respiratory factor 1 (NRF1) and two miRNAs were predicted to be regulators of the hub genes. In summary, Csf2 may serve as a novel diagnostic and therapeutic target for ALI. NRF1 and mmu-mir-122-5p may be key regulators in the development of ALI.

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