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Mast cells (MCs) are hematopoietic cells that reside ubiquitously in all vascularized tissues. They are potential sources of a wide variety of biologically active secreted compounds, including diverse cytokines, chemokines and growth factors. In addition, they participate in innate and adaptive immune responses. MCs are the most important cells in immediate reactions and chronic IgE-associated allergic disorders and enhance the host resistance to certain biological agents, including viruses. Therefore, MCs influence many biological responses to viruses and other microbiological agents. Viruses activate MCs through TLR4 leading to the generation of several pro-inflammatory cytokines, including those of the IL-1 family. Here, we report how viruses can activate MCs producing severe inflammation and how these interesting cells can activate the immune system by carrying out a protective action for our organism.
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Literature suggests that sEMG (surface Electromiography) of stomatognathic muscles is different in subjects with open eyes and closed eyes in various pathological conditions. Ultra-Low Frequency Transcutaneous Nervous Stimulation (ULF TENS) is used in dentistry to evaluate the adaptation capacity of the autonomic and muscular system and, at the same time, some self-assessment scales (CSI and DASS42) can help the dentist to evaluate the state of central hypo-excitability/ dysregulation. The aim of this paper is to evaluate ULF TENS effect in condition of opened eyes and closed eyes and to link the sEMG response to Central Sensitization condition or psychological condition of evaluation scales score. 27 healthy patients have been analyzed with 8 channels sEMG. Four homologue muscle couples (masseters, anterior digastrics, sternocleidomastoid, and anterior temporalis) in condition of open eyes and closed eyes before and after ULF TENS were checked, after the compilation of CSI and DASS42 scales. Left Temporal Anterior sEMG scores with open eyes are significantly higher than those obtained with closed eyes. The increasing answer of electric tone is higher on the left side. After ULF TENS the left side muscles activation is reduced and this response to stimulation is inversely proportional to CSI and DASS42 scores. ULF TENS is highly effective on those patients acting on the nucleus for coupling between sensory stimulus and modulation of the autonomous behavioral response.
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Breast cancer (BC) is one of the most common tumors and the second leading cause of cancer-related death among women. Long non-coding RNA (lncRNA) is vital in regulating the progression of BC, however, its biological function in BC is inconclusive. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to quantify the expressions of LINC01088, microRNA (miRNA) miR-498, phosphatase and tensin homologue deleted on chromosome 10 (PTEN) mRNA in BC tissues and cells. Cell counting kit-8 (CCK-8) and 5-Ethynyl-2’-deoxyuridine (EdU) assays were used to detect cell proliferation. The apoptosis was detected by flow cytometry. Moreover, PTEN protein expression was determined by Western blot. Dual-luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay were used to verify the targeting relationships among LINC01088, miR-498, and PTEN. LINC01088 expression level was declined in BC tissues and cells, which was related to higher TNM stage. LINC01088 overexpression significantly inhibited the growth of BC cells, induced apoptosis, promoted Bax and cleaved-caspase-3 expressions, and restrained Bcl-2 expression; LINC01088 knockdown worked oppositely. MiR-498 was confirmed as the target of LINC01088. PTEN expression was negatively modulated by miR-498 and positively regulated by LINC01088 in BC cells. LINC01088 up-regulates the expression of PTEN by targeting miR-498 and has the potential to repress the progression of BC.
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Colon cancer is a highly malignant gastrointestinal cancer, and genes in the tumor infiltrating cells and microenvironment are emerging as pivotal players in its development and prognosis. In this study, TIMER and StarBase tools were used to find whether EIF4E3 gene was downregulated in colon tissues, and whether lower expression of EIF4E3 was associated with poor prognosis in colon cancer patients, as well as to ascertain that EIF4E3 could regulate immune-related pathways by gene set enrichment analysis (GSEA). Using TIMER (Tumor Immune Estimation Resource) database and ImmuneCellAI tools, it was found that EIF4E3 expression was correlated with tumor immune infiltrates in colon cancer. The results identified EIF4E3 as an immune infiltrate-correlated prognosticator in colon cancer.
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BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B) belongs to the spindle assembly checkpoint protein family and is linked to the pathogenesis of diverse human cancers. This work intends to probe its expression, function and underlying molecular mechanism in ovarian cancer (OC). In the present work, gene expression profiles of GSE14407, GSE18520, and GSE54388 were obtained from the GEO database and screened for differentially expressed genes (DEGs) in ovarian cancer tissues. KM-plotter database was employed to analyze the relationship between BUB1B expression and the prognosis of OC patients. Immunohistochemistry was utilized to examine BUB1B expression in OC tissues and adjacent ovarian tissues. BUB1B expression level in OC cells was also examined using qRT-PCR. The relationship between BUB1B expression and clinicopathological parameters in OC patients was analyzed using the Chi-squared test. CCK-8 and BrdU experiments were employed to examine cell proliferation. Cell migration and invasion were detected by Transwell experiment. Western blot, qRT-PCR and dual-luciferase reporter gene analyses were employed to validate the regulatory relationship between miR-486-5p and BUB1B. In this work, we demonstrated that BUB1B was remarkably overexpressed in OC specimens compared with adjacent nontumor tissue, which was associated with higher FIGO stage and differentiation status of the patients. OC cell proliferation, migration and invasion were substantially enhanced by BUB1B overexpression; conversely, knocking down BUB1B worked the opposite effect. Mechanistically, BUB1B was one of the downstream targets of miR-486-5p and was negatively modulated by the latter. It was concluded that,BUB1B, negatively regulated by miR-486-5p, facilitates OC progression, which is a promising target for OC therapy.
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Osteosarcoma (OS) is a rare malignant tumor derived from bone cells. Many studies have reported that metastatic OS is associated with a poorer prognosis. However, there are no current effective methods of predicting survival. We applied gene expression data of OS from Gene Expression Omnibus (GEO) and Therapeutically Applicable Research to Generate Effective Treatments (TARGET) to identify hub genes and construct a risk model with the help of R software. We then verified the identified signature using GEO data. Then we explored the potential relationship between the risk score and immune microenvironment in OS. After a series of analyses, we identified four hub-genes (APBB1IP, UHRF2, PDK1 and CORT). Hub genes were then used to construct a model using a training data set. The model was subsequently tested using a validation data set, and performed well in sensitivity and specificity. In the immune analysis, we found the high-risk score might represent immunosuppression in OS. The identified hub genes may play a critical role in the mechanism of the metastatic OS. Moreover, the model we built was related to immunosuppression in OS. Thus, the gene signature identified could be a potential target for future clinical treatment of OS.
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Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders associated with immunity and inflammation. However, the underlying immune/inflammation-related molecular characteristics of PCOS, such as miRNAs, lncRNAs remain unclear. The aim of this study was to investigate the immune-related biomarkers in PCOS based on the competitive endogenous RNA (ceRNA) mechanism. We analyzed the differential expression (DE)-mRNAs, DE-miRNAs and DE-LncRNA based on datasets GSE155489 and GSE138572. Functional enrichment analysis was performed on immune/inflammationrelated pathways of DE-mRNAs. Furthermore, an immune/inflammation-related ceRNA network was constructed based on the DE-mRNAs, DE-miRNAs and DE-lncRNAs. For further validation, qRT-PCR was used to detect the expression level of the upregulated candidate LncRNAs. In addition, receiver operating characteristics (ROC) were constructed to evaluate the diagnostic value of the LncRNAs. We identified 5 lncRNAs as the potential immune/inflammation-related biomarkers of PCOS, including KCTD21-AS1, SNHG12, CRNDE, FAM157C and AC111152.2. AC111152.2 has the best performance with an area of 0.831. Our results provided novel insights into the discovery of immune/inflammation-related genetic biomarkers for PCOS. However, their specific regulatory mechanisms still need to be further studied.
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This research aims to probe the effect and mechanism of microRNA-138-5p (miR-138-5p) in regulating oxidized low-density lipoprotein (Ox-LDL)-induced lipid peroxidation of vascular endothelial cells (VECs). The miR-138-5p profile in the serum of 50 atherosclerosis (AS) patients and 50 healthy donors was compared by reverse transcription-polymerase chain reaction (RT-PCR). VECs were treated with Ox-LDL to construct a model of lipid peroxidation injury in vitro. miR-138-5p mimics and inhibitors or the corresponding negative controls were transfected into VECs. CCK-8 and BrdU methods were used to detect the viability of VECs. RT-PCR and Western blot (WB) were implemented to test inflammatory cytokines (TNF-α, IL-1β, IL-6), SIRT1, COX2, iNOS, STAT6, NF-κB, Caspase3, Bcl2, Bax, MMP3, MMP9, ICAM1, VCAM1, and LOX1, respectively. Moreover, the relevancy between miR-138-5p and SIRT1 was validated by bioinformatics analysis and further testified by dual-luciferase reporter assay. As the data indicated, miR-138-5p was up-regulated in the serum of AS patients and exhibited a positive correlation with the plasma LDL level. In vitro, overexpressing miR-138-5p promoted Ox-LDL-mediated VECs apoptosis, inhibited cell viability and angiogenesis, aggravated inflammation, attenuated the expression of STAT6 and promoted NF-κB pathway activation, whereas miR-138-5p inhibition exerted the opposite effects. Mechanistically, miR-138-5p targeted the 3’untranslated region (3 ‘-UTR) of SIRT1 and negatively regulated SIRT1. Moreover, knocking down SIRT1 distinctly reversed miR-138-5p inhibitor-mediated antiapoptosis and anti-inflammatory effects against Ox-LDL. Collectively, inhibiting miR-138-5p attenuated Ox-LDL-modulated VEC injury and inflammation by regulating the SIRT1/NF-κB pathway.
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This study was aimed to explore the molecular basis underlying the therapeutic effects of β-hydroxybutyrate in cardiac hypertrophy. We established a model of cardiomyocyte hypertrophy in H9c2 cells induced by angiotensin II (AngII). The anti-hypertrophic effects of β-hydroxybutyrate were evaluated by assessing cell apoptosis and expression levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and nuclear factor of activated T-cells 1 (NFATc1). The miRNA-mRNA network and associated functional analyses were performed based on miRNA sequencing data. Expression levels of six miRNAs involved in the miRNA-mRNA network were evaluated using quantitative real-time polymerase chain reaction (qRT-PCR). Eight mM β-hydroxybutyrate significantly attenuated AngIIinduced cell apoptosis and significantly decreased the AngII-induced upregulation of ANP (p < 0.01), BNP (p < 0.01), and NFATc1 (p < 0.01). Based on the miRNA sequencing data, 1327 miRNA-mRNA pairs were screened, including miR-672-3p, miR-760-5p, miR-6325, miR-3583-3p, miR-3065-3p, and miR-3541. Functional analysis revealed that target genes were significantly enriched in four KEGG pathways, including the Wnt signaling pathway, tumor necrosis factor (TNF) signaling pathway, adherens junction, and Hippo signaling pathway. These genes were significantly enriched in eight biological processes, including protein deneddylation, amino acid transmembrane transport, and amino acid transport. Following treatment with β-hydroxybutyrate, the expression levels of miR-672-3p, miR760-5p, miR-3583-3p, miR-3065-3p, and miR-3541 were significantly upregulated, and miR-6325 was significantly downregulated when compared with AngII treatment. Our data confirmed the protective role of β-hydroxybutyrate on cardiac hypertrophy, providing insights into observed therapeutic effects.
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The present study aimed to explore changes in serum betatrophin concentration in women with gestational diabetes mellitus (GDM) and its relationship with clinical metabolic indicators. The research also aimed to provide a basis for the in-depth study of the pathogenesis of GDM, together with a new target for the treatment of the condition and improving the methods for its prediction and diagnosis. A total of 60 participants were included of whom 30 were enrolled in the pregnancy with normal glucose regulation (P-NGR) group, and 30 in the GDM group. The clinical metabolic indicators in the two groups were measured and body mass index (BMI) was calculated. Additionally, two models were established, i.e., homeostasis assessment of insulin resistance (HOMA-IR), and homeostasis assessment of beta-cell function (HOMA-β). An enzyme-linked immunosorbent assay (ELISA) was used to detect the serum betatrophin concentrations in the two groups. The differences in the clinical metabolic indicators and betatrophin concentrations between the two groups were compared, and the correlation between betatrophin and clinical metabolic indicators was analyzed. The receiver operating characteristic (ROC) curve was used to predict GDM using the serum betatrophin concentration. The levels of triglyceride (TG) (P = 0.001), total cholesterol (TC) (P = 0.004), low-density lipoprotein (LDL) (P < 0.001), fasting blood glucose (FBG) (P < 0.001), fasting serum insulin (FSI) (P = 0.028), HOMA-IR (P < 0.001), HOMA-β (P < 0.001), and the concentration of betatrophin (p < 0.001) were significantly higher in the GDM compared with the P-NGR group, and the difference was statistically significant. The concentration of betatrophin was positively correlated with BMI (P = 0.017), TG (P = 0.005), TC (P = 0.018), FSI (P = 0.023), and HOMA-IR (P = 0.022) in the GDM group. Multiple linear regression analysis showed that HOMA-IR and TG could affect the serum betatrophin concentration. The best cut-off point of the serum betatrophin concentration predicted by the ROC curve in the case of GDM was 800.1pg/ml. The serum concentration of betatrophin in the GDM group was significantly increased and positively correlated with BMI, TG, TC, FSI, and HOMA-IR. Insulin resistance in the GDM population may be a mechanism involved in the overexpression of serum betatrophin; therefore, serum betatrophin could potentially be used as a biochemical indicator for predicting GDM.
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Pulmonary fibrosis (PF) may be reduced by inducing autophagy, and miR-128-3p could regulate cell autophagy through several methods, however, the mechanism is still unknown. In this experiment, whether miR-128-3p could regulate the bleomycin-induced autophagy of MRC-5 cells by regulating the PTEN/AKT/GSK3β/mTOR signaling pathway was explored. Bleomycin (10 μg/mL) was used to induce MRC-5 cells in vitro and form a cell model of PF. The relative proliferation rate, activity, and autophagy rate of MRC-5 cells were detected using MTT, CCK-8, and GFP-LC3 fluorescence, respectively. The expression levels of LC3-II, Beclin-1, PTEN, p-Akt, p-GSK3β, and p-mTOR proteins in bleomycin-induced MRC-5 cells were determined via Western blotting. The expression levels of GSK3β mRNA and miR-128-3p were determined in bleomycin-induced MRC-5 cells through real-time polymerase chain reaction. The results showed that bleomycin decreased the autophagy of MRC-5 cells and increased the activity and proliferation rate of these cells. The miR-128-3p inhibitor inhibited the expression levels of p-Akt and p-mTOR, increased the expression levels of GSK3β, PTEN, LC3-II, and Beclin-1, and induced bleomycin-induced autophagy in MRC-5 cells. The results suggested that miR-128-3p overexpression could improve bleomycin-induced PF by increasing the bleomycin-induced autophagy of MRC-5 cells. The mechanism may be related to the decreased expression of GSK3β gene and protein by upregulating miR-128-3p expression.
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Neonatal respiratory distress syndrome (NRDS) is a leading cause of neonatal mortality, and commonly occurs in preterm neonates. Vitamins are closely related with lung development. The purpose of this study was to evaluate the clinical predictive value of umbilical cord serum vitamins A, D and E for NRDS onset in both preterm and term infants. A total of 150 NRDS neonates, including 114 preterm and 36 term cases, were included in this study. The levels of vitamins A, D and E in the umbilical cord serum of NRDS neonates were measured using electrochemiluminescence method. The predictive value of vitamins was evaluated using logistics regression analysis and receiver operating characteristic curves. Vitamins A, D and E levels were significantly reduced in NRDS neonates and served as risk factors for the onset of NRDS with certain predictive accuracy, which manifested by the area under the curve (AUC) value (0.885 for vitamins A, 0.875 for vitamins D, 0.720 for vitamins E). Additionally, in the 114 preterm cases, decreased vitamins A, D and E were also independently associated with NRDS occurrence. For term NRDS neonates, only vitamins A and D were determined as two risk factors for disease onset. Overall, vitamins A, D and E levels were lower in NRDS compared with normal control neonates, and vitamins A and D played as predictive indicators for NRDS onset in both preterm and term neonates, while relationship between vitamins E and NRDS was only found in preterm neonates.
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To investigate the effect and probable mechanism of triggering receptor expressed on myeloid cells-1 (TREM-1) inhibition of hyperactive Kupffer cells (KCs) on acute liver injury caused by severe heat stroke (HS). A total of 32 rats were randomized into the LP17, GdCl3, control (CON), and heat stroke (HS) groups. Serum ALT and AST activities in each group were assessed. Additionally, liver tissues were obtained to examine cellular structure, determine superoxide dismutase (SOD) concentrations, analyze apoptosis, and determine the expression levels of TREM-1, TREM-2, DAP12, TNF-α, and IL-6 in KCs, as well as Bcl-2, Bax, CleveadCaspase3, and Clevead-Caspase9 in liver. Results of the study showed that compared to the CON group, the HS group had higher serum AST and ALT levels, with more serious pathological changes. Hepatocyte apoptosis and lysosome formation in KCs increased when heatstroke occurred, while SOD concentrations decreased. Moreover, expression levels of TREM-1, DAP12, TNF-α, IL-6, Bax, Clevead-Caspase3, and Clevead-Caspase9 increased in the HS group, while TREM-2 and Bcl-2 expression levels decreased. Pretreatment with LP17 and GdCl3 significantly ameliorated the aforementioned indicators, relieving acute liver injury caused by heat stroke. The results of this study showed that Inhibiting TREM-1 of KCs improved severe HS-induced liver injury, which involved an underlying mechanism of regulating the imbalance of expressions in the TREMs/DAP12 pathway. Thus, inhibiting KC activities improved antioxidant consumption and alleviated apoptosisrelated protein overexpression, thereby reducing HS-induced hepatocyte apoptosis.
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This study was carried out to identify the metabolic and prognostic molecular subtypes and corresponding molecular markers of oral squamous cell carcinoma (OSCC) based on the OSCC data on The Cancer Genome Atlas (TCGA). UCSC Xena and NCBI GEO database were used to obtain RNA-seq data. The single-factor Cox regression analysis and unsupervised consensus cluster analysis were employed to screen metabolic genes and identify clusters. Survival analysis and clinicopathological analysis were used to analyze the differences of clusters. The limma package was used to obtain featured genes. Database for Annotation, Visualization and Integrated Discovery (DAVID) software was utilized to analyze the Gene Ontology Biological Processes (GO-BP) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway of each featured gene. STRING database, Cytoscape and CytoNCA were applied to Protein-protein interaction (PPI) network construction and module analysis. GSE42743 data set was applied to genes and cluster validation. A total of 54 genes were obtained as metabolic and prognosis-related genes and 4 clusters were divided. Survival rate in cluster4 and cluster1 is significantly higher than cluster3 and cluster2, and the formation of these clusters is only related to metabolic molecules. Different numbers of featured genes were obtained in clusters and a large number of functional signaling pathways were enriched. PPI network showed a total of 338 relationship pairs and 128 genes corresponding to proteins. and then 8 hub genes were identified. The feasibilities of 6 screened molecular markers of cluster1 were successfully verified by GSE42743 data set. OSCC was divided into 4 clusters through bioinformatics analysis. There are survival differences between these four clusters. A total of 6 molecular markers were identified in cluster1 for cluster identification of OSCC.
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The purpose of the study was to investigate the clinical efficacy and adverse reactions of dexamethasone combined with ademetionine in the treatment of intrahepatic cholestasis of pregnancy (ICP). Ninety-four patients with ICP admitted to our hospital from February 2018 to February 2019 were selected and were randomly divided into control group (n=47) and experimental group (n=47). Among them, the patients in the control group were treated with routine ademetionine for therapeutic intervention, while the patients in the experimental group were treated with dexamethasone combined with ademetionine. After that, the clinical efficacy, and adverse reactions of these two treatment methods were compared between the two groups. The pruritus scores of the patients in the two groups after treatment were significantly lower than those before treatment, and the scores in the experimental group were significantly lower than those in the control group. The levels of liver function indexes such as AST, ALT and TBA in both groups after treatment were significantly lower than those before treatment, and the levels in the experimental group were significantly lower than those in the control group. The levels of proinflammatory cytokines such as IL-12 and TNF-α in both groups after treatment were lower than those before treatment, and those levels after treatment in the experimental group were significantly lower than those in the control group, with statistically significant differences (all P < 05). There were no adverse reactions such as nausea, vomiting, abdominal pains, etc. occurring in the two groups during the treatment. Patients’ electrocardiogram and blood and urine routine examination results were normal and medication safety was ensured. Dexamethasone combined with ademetionine can effectively relieve pruritus, reduce the levels of proinflammatory cytokines and improve liver function indexes, with no obvious adverse reactions in the treatment, which is worthy of application and promotion in the clinical practice.
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Mesenchymal stem cells (MSCs) are known to migrate to tumor tissues and play an important role in cancer progression. However, the effects of MSCs on tumor progression remain controversial. The aim of our study was to detect the effects of human umbilical cord blood-derived MSCs (hUCB-MSCs) on the human ovarian cancer SKOV3 cell line in vitro and the underlying mechanisms. MSCs were isolated from blood of umbilical vein in full-term healthy deliveries. SKOV3 cells were treated with conditioned medium (CM) from hUCB-MSCs. The CCK-8 (Cell Counting Kit) assay was used to determine the effect on proliferation. AnnexinV-FITC/PI staining was used to detect the cell cycle and apoptosis. Caspase-Glo®3/7 assay kit was used to detect the expression of caspase3/7 protein. Autophagy levels were determined based on expression of autophagic marker LC3, StubRFP-SensGFP-LC3 analysis, and electron microscopy. hUCB-MSCs are characteristically similar to other sources of MSCs, which are inconsistent with previous reports and exhibit multipotential differentiation capability (adipocytes and osteoblasts). The CCK-8 result revealed that hUCB-MSCs-CM inhibited the proliferation than those observed in the control group. Analysis of the cell cycle indicated that hUCB-MSCs-CM significantly increased the percentage of SKOV3 cells in the G2/M phase compared with the Ctrl group. Flow cytometry analysis and Caspase-Glo 3/7 Assay suggested that hUCB-MSCs-CM promoted apoptosis. hUCB-MSCs-CM increased LC3-II levels as well as autophagosome number in SKOV3 cells. These results indicate that hUCB-MSCs significantly inhibited the proliferation of SKOV3 cells in vitro, which is possibly due to blocking its cell cycle at G2/M phase and inducing SKOV3 cell death through synergistic apoptosis and autophagy. This theoretically supports hUCB-MSCs as an effective anticancer adjuvant in the treatment of ovarian cancer.
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Steroid-induced osteonecrosis of the femoral head (SONFH) is a severe disease. Nonetheless, the pathogenesis of SONFH is not fully understood, and it is challenging to make an early diagnosis. This study aimed to explore the hallmark genes associated with SONFH and predict potential biomarkers for SONFH. The microarray dataset GSE123568 was obtained from the Gene Expression Omnibus (GEO) database. The Weighted Gene Co-expression Network Analysis (WGCNA) and limma R-package were used to screen the intersection genes between the interest module genes and differential expression genes (DEGs). A protein-protein interaction (PPI) network, cross-talk, and receiver operating characteristic (ROC) curve were utilized to identify the optimal hallmark genes. The Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Set Variation Analysis (GSVA), and Gene Set Enrichment Analysis (GSEA) were performed to explore the potential molecular mechanism of genes. The single-sample Gene Set Enrichment Analysis (ssGSEA) and CIBERSORT algorithm were used to analyze the immune infiltration level in SONFH. There were 96 intersection genes acquired between the interest module and DEGs. Based on the PPI network, cross-talk, and ROC curve analysis, we identified 6 SONFH-related hallmark genes, including TYROBP, TLR8, TLR2, LILRB2, HCK, and TREM1, which showed heterogeneous biological functions or molecular mechanisms. The Toll-like receptor (TLR) signaling pathway was considered the primary pathway in the development of SONFH. Finally, we found that the neutrophils might be the culprit in the SONFH. Our study identified some SONFH-related hallmark genes and revealed novel insights into the biological mechanism of SONFH, which provided a theoretical foundation for further experimental study and contributed to understanding the pathogenesis of SONFH.
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