Bcl-2 Is Involved in Cardiac Hypertrophy through PI3K-Akt Pathway

Cardiac hypertrophy (CH) is a common cause of sudden cardiac death and heart failure, resulting in a significant medical burden. The present study is aimed at exploring potential CH-related pathways and the key downstream effectors. The gene expression profile of GSE129090 was obtained from the Gene Expression Omnibus database (GEO), and 1325 differentially expressed genes (DEGs) were identified, including 785 upregulated genes and 540 downregulated genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Reactome pathway enrichment analysis of DEGs were then performed. Although there were no pathways enriched by downregulated genes, many CH-related pathways were identified by upregulated genes, including PI3K-Akt signaling pathway, extracellular matrix- (ECM-) receptor interaction, regulation of actin cytoskeleton, and hypertrophic cardiomyopathy (HCM). In the deeper analysis of PI3K-Akt signaling pathway, we found all the signaling transduction pointed to B cell lymphoma-2- (Bcl-2-) mediated cell survival. We then demonstrated that PI3K-Akt signaling pathway was indeed activated in cardiac hypertrophy. Furthermore, no matter LY294002, an inhibitor of the PI3K/AKT signaling pathway, or Venetoclax, a selective Bcl-2 inhibitor, protected against cardiac hypertrophy. In conclusion, these data indicate that Bcl-2 is involved in cardiac hypertrophy as a key downstream effector of PI3K-Akt signaling pathway, suggesting a potential therapeutic target for the clinical management of cardiac hypertrophy.

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Effects of Fibronectin 1 on Cell Proliferation, Senescence and Apoptosis of Human Glioma Cells Through the PI3K/AKT Signaling Pathway

Cellular Physiology and Biochemistry ◽

10.1159/000492096 ◽

2018 ◽

Vol 48 (3) ◽

pp. 1382-1396 ◽

Cited By ~ 39

Author(s):

Yu-Xiang Liao ◽

Zhi-Ping Zhang ◽

Jie Zhao ◽

Jing-Ping Liu

Keyword(s):

Gene Expression ◽

Cell Cycle ◽

Cell Proliferation ◽

Signaling Pathway ◽

Enrichment Analysis ◽

Akt Signaling ◽

Pathway Enrichment Analysis ◽

Akt Signaling Pathway ◽

Go Enrichment ◽

Go Enrichment Analysis

Background/Aims: The current study aimed to investigate the role by which fibronectin 1 (FN1) influences the cell cycle, senescence and apoptosis in human glioma cells through the PI3K/ AKT signaling pathway. Methods: Differentially expressed genes (DEGs) were identified based on gene expression data (GSE12657, GSE15824 and GSE45921 datasets) and probe annotation files from Gene Expression Omnibus. The DEGs were identified in connection with gene ontology (GO) enrichment analysis and with the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. The positive expression of the FN1 protein was detected by immunohistochemistry. The glioma cell lines U251 and T98G were selected and assigned into blank, negative control (NC) and siRNA-FN1 groups. A dual luciferase reporter gene assay was used to investigate the effects of FN1 on transcriptional activity through the PI3K/AKT signaling pathway. An MTT assay was applied for the detection of cell proliferation, while flow cytometry was employed for cell cycle stage and cellular apoptosis detection. β-galactosidase staining was utilized to detect cellular senescence, a scratch test was applied to evaluate cell migration, and a transwell assay was used to analyze cell invasion. Western blotting and qRT-PCR methods were used to detect the protein and mRNA expression levels, respectively, of the FN1 gene and the related genes in the PI3K/AKT pathway (PI3K, AKT and PTEN), the cell cycle (pRb, CDK4 and Cyclin D1) and cell senescence (p16 and p21) among the collected tissues and cells. Results: GSE12657 profiling revealed FN1 to be the most upregulated gene in glioma. Regarding the GSE12657 and GSE15824 datasets, FN1 gene expression was higher in glioma tissues than in normal tissues. GO enrichment analysis and KEGG pathway enrichment analysis indicated that FN1 is involved in the synthesis of extracellular matrix (ECM) components and the PI3K/AKT signaling pathway. Verification was provided, indicating the role played by the FN1 gene in the regulation of the PI3K/AKT signaling pathway, as silencing the FN1 gene was found to inhibit cell proliferation, promote cell apoptosis and senescence, and reduce migration and invasion through the down-regulation of FN1 gene expression and disruption of the PI3K-AKT signaling pathway. Conclusion: The findings of this study provide evidence highlighting the prominent role played by FN1 in stimulating glioma growth, invasion, and survival through the activation of the PI3K/AKT signaling pathway.

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Analyzing gene expression profiles with preliminary validations in cardiac hypertrophy induced by pressure overload

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2017-0585 ◽

2018 ◽

Vol 96 (8) ◽

pp. 701-709 ◽

Cited By ~ 1

Author(s):

Jing Gao ◽

Yuhong Li ◽

Tongmei Wang ◽

Zhuo Shi ◽

Yiqi Zhang ◽

...

Keyword(s):

Gene Expression ◽

Cardiac Hypertrophy ◽

Expression Profiles ◽

Gene Expression Profiles ◽

Pressure Overload ◽

Enrichment Analysis ◽

Receptor Interaction ◽

Pathway Enrichment Analysis ◽

Ontology Term ◽

The Common

The aim of this study was to identify the key genes involved in the cardiac hypertrophy (CH) induced by pressure overload. mRNA microarray data sets GSE5500 and GSE18801 were downloaded from the Gene Expression Omnibus database, and differentially expressed genes (DEGs) were screened using the Limma package; then, functional and pathway enrichment analysis were performed for common DEGs using the Database for Annotation, Visualization and Integrated Discovery database. Furthermore, the top DEGs were further validated using quantitative PCR in the hypertrophic heart tissue induced by isoprenaline. A total of 113 common DEGs with absolute fold change > 0.5, including 60 significantly upregulated DEGs and 53 downregulated DEGs, were obtained. Gene ontology term enrichment analysis suggested that common upregulated DEG were mainly enriched in neutrophil chemotaxis, extracellular fibril organization, and cell proliferation; and the common downregulated genes were significantly enriched in ion transport, endoplasmic reticulum, and dendritic spine. Kyoto Encyclopedia of Genes and Genomes pathway analysis found that the common DEGs were mainly enriched in extracellular matrix receptor interaction, phagosome, and focal adhesion. Additionally, the expression of Mfap4, Ltbp2, Aspn, Serpina3n, and Cnksr1 were upregulated in the model of CH, while the expression of Anp32a was downregulated. The current study identified the key deregulated genes and pathways involved in the CH, which could shed new light to understand the mechanism of CH.

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Elaborate the Mechanism of Ancient Classic Prescriptions (Erzhi Formula) in Reversing GIOP by Network Pharmacology Coupled with Zebrafish Verification

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2022/7019792 ◽

2022 ◽

Vol 2022 ◽

pp. 1-17

Author(s):

Zhihui Cai ◽

Huajun Wang ◽

Jun Jiang ◽

Shichang Xiao ◽

Jianpeng Xiao ◽

...

Keyword(s):

Signaling Pathway ◽

Optical Density ◽

Bone Mineralization ◽

Enrichment Analysis ◽

Akt Signaling ◽

Network Pharmacology ◽

Pathway Enrichment Analysis ◽

Akt Signaling Pathway ◽

Active Components ◽

Zebrafish Model

Osteoporosis is a degenerative disease that endangers human health. At present, chemical drugs used for osteoporosis have serious side effects. Therefore, it is valuable to search herbs with high safety and good curative effect in antiosteoporosis. Erzhi formula (EZF), an ancient classic compound, has been reported to have a beneficial effect in antiosteoporosis, but its mechanism is unclear. In this paper, the active compounds of EZF were found in Systems Pharmacology Database, and gene targets related to osteoporosis were obtained in GeneCards. The GO functional and KEGG pathway enrichment analysis were performed by Metascape. The network of “components-targets-signal pathway” was constructed by Cytoscape. Next, molecular docking between the active components and hub genes related to the PI3K-Akt signaling pathway was conducted by Autodock. In the verification experiment, the zebrafish induced by prednisolone (PNSL) was used to reproduce glucocorticoid-induced osteoporosis (GIOP) model, and then the reversal effects of EZF were systematically evaluated according to the behavior, skull staining area, bone mineralization area (BMA), average optical density (AOD), and cumulative optical density (COD). Finally, it was shown that 24 components in EZF could regulate 39 common gene targets to exert antiosteoporosis effect. Besides, the main regulatory mechanisms of EZF were 4 signaling pathways: PI3K-Akt, JAK-STAT, AGE-RAGE, and cancer pathway. In PI3K-Akt signaling pathway, wedelolactone, dimethyl wedelolactone, specnuezhenide, ursolic acid, acacetin, beta-sitosterol, apigenin, and kaempferol can bind tightly with EGF, IL-2, and IL-4 genes. Compared with the model group, the moving distance, swimming speed, and cumulative swimming time of zebrafish in EZF group were significantly increased ( P < 0.05 ). Meanwhile, the BMA and COD of zebrafish were significantly improved after the intervention of EZF ( P < 0.05 ). In summary, the 24 components of EZF exert their antiosteoporosis effects by regulating 39 related gene targets, among which the PI3K signaling pathway is crucial. EZF can promote bone formation and reversed GIOP through “multicomponent/multitarget/multipathway” and the medium dose of EZF may be the most suitable concentration for the treatment of GIOP in zebrafish model.

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AB0005 IDENTIFICATION OF KEY GENES AND PATHWAYS FOR PSORIASIS BASED ON GEO DATABASES BY BIOINFORMATICS ANALYSIS

Annals of the Rheumatic Diseases ◽

10.1136/annrheumdis-2021-eular.1773 ◽

2021 ◽

Vol 80 (Suppl 1) ◽

pp. 1037.2-1038

Author(s):

X. Sun ◽

S. X. Zhang ◽

S. Song ◽

T. Kong ◽

C. Zheng ◽

...

Keyword(s):

Gene Expression ◽

Signaling Pathways ◽

Differentially Expressed Genes ◽

Enrichment Analysis ◽

Differentially Expressed ◽

Shanxi Province ◽

Receptor Interaction ◽

Term Therapy ◽

Pathway Enrichment Analysis ◽

Key Genes

Background:Psoriasis is an immune-mediated, genetic disease manifesting in the skin or joints or both, and also has a strong genetic predisposition and autoimmune pathogenic traits1. The hallmark of psoriasis is sustained inflammation that leads to uncontrolled keratinocyte proliferation and dysfunctional differentiation. And it’s also a chronic relapsing disease, which often necessitates a long-term therapy2.Objectives:To investigate the molecular mechanisms of psoriasis and find the potential gene targets for diagnosis and treating psoriasis.Methods:Total 334 gene expression data of patients with psoriasis research (GSE13355 GSE14905 and GSE30999) were obtained from the Gene Expression Omnibus database. After data preprocessing and screening of differentially expressed genes (DEGs) by R software. Online toll Metascape3 was used to analyze Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of DEGs. Interactions of proteins encoded by DEGs were discovered by Protein-protein interaction network (PPI) using STRING online software. Cytoscape software was utilized to visualize PPI and the degree of each DEGs was obtained by analyzing the topological structure of the PPI network.Results:A total of 611 DEGs were found to be differentially expressed in psoriasis. GO analysis revealed that up-regulated DEGs were mostly associated with defense and response to external stimulus while down-regulated DEGs were mostly associated with metabolism and synthesis of lipids. KEGG enrichment analysis suggested they were mainly enriched in IL-17 signaling, Toll-like receptor signaling and PPAR signaling pathways, Cytokine-cytokine receptor interaction and lipid metabolism. In addition, top 9 key genes (CXCL10, OASL, IFIT1, IFIT3, RSAD2, MX1, OAS1, IFI44 and OAS2) were identified through Cytoscape.Conclusion:DEGs of psoriasis may play an essential role in disease development and may be potential pathogeneses of psoriasis.References:[1]Boehncke WH, Schon MP. Psoriasis. Lancet 2015;386(9997):983-94. doi: 10.1016/S0140-6736(14)61909-7 [published Online First: 2015/05/31].[2]Zhang YJ, Sun YZ, Gao XH, et al. Integrated bioinformatic analysis of differentially expressed genes and signaling pathways in plaque psoriasis. Mol Med Rep 2019;20(1):225-35. doi: 10.3892/mmr.2019.10241 [published Online First: 2019/05/23].[3]Zhou Y, Zhou B, Pache L, et al. Metascape provides a biologist-oriented resource for the analysis of systems-level datasets. Nat Commun 2019;10(1):1523. doi: 10.1038/s41467-019-09234-6 [published Online First: 2019/04/05].Acknowledgements:This project was supported by National Science Foundation of China (82001740), Open Fund from the Key Laboratory of Cellular Physiology (Shanxi Medical University) (KLCP2019) and Innovation Plan for Postgraduate Education in Shanxi Province (2020BY078).Disclosure of Interests:None declared

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Capn4 aggravates angiotensin II-induced cardiac hypertrophy by activating the IGF-AKT signaling pathway

The Journal of Biochemistry ◽

10.1093/jb/mvab100 ◽

2021 ◽

Author(s):

Yuanping Cao ◽

Qun Wang ◽

Caiyun Liu ◽

Wenjun Wang ◽

Songqing Lai ◽

...

Keyword(s):

Angiotensin Ii ◽

Cardiac Hypertrophy ◽

Signaling Pathway ◽

Expression Patterns ◽

Akt Signaling ◽

Calpain Inhibitor ◽

Ang Ii ◽

Akt Signaling Pathway ◽

Calpain Activity

Abstract Capn4 belongs to a family of calpains that participate in a wide variety of biological functions, but little is known about the role of Capn4 in cardiac disease. Here, we show that the expression of Capn4 was significantly increased in Angiotensin II (Ang II)-treated cardiomyocytes and Ang II-induced cardiac hypertrophic mouse hearts. Importantly, in agreement with the Capn4 expression patterns, the maximal calpain activity measured in heart homogenates was elevated in Ang II-treated mice, and oral coadministration of SNJ-1945 (calpain inhibitor) attenuated the total calpain activity measured in vitro. Functional assays indicated that overexpression of Capn4 obviously aggravated Ang II-induced cardiac hypertrophy, whereas Capn4 knockdown resulted in the opposite phenotypes. Further investigation demonstrated that Capn4 maintained the activation of the insulin-like growth factor (IGF)-AKT signaling pathway in cardiomyocytes by increasing c-Jun expression. Mechanistic investigations revealed that Capn4 directly bound and stabilized c-Jun, and knockdown of Capn4 increased the ubiquitination level of c-Jun in cardiomyocytes. Additionally, our results demonstrated that the antihypertrophic effect of Capn4 silencing was partially dependent on the inhibition of c-Jun. Overall, these data suggested that Capn4 contributes to cardiac hypertrophy by enhancing the c-Jun-mediated IGF-AKT signaling pathway and could be a potential therapeutic target for hypertrophic cardiomyopathy.

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A77 1726 (leflunomide) blocks and reverses cardiac hypertrophy and fibrosis in mice

Clinical Science ◽

10.1042/cs20180160 ◽

2018 ◽

Vol 132 (6) ◽

pp. 685-699 ◽

Cited By ~ 20

Author(s):

Zhen-Guo Ma ◽

Xin Zhang ◽

Yu-Pei Yuan ◽

Ya-Ge Jin ◽

Ning Li ◽

...

Keyword(s):

T Cell ◽

Cardiac Hypertrophy ◽

Protective Effect ◽

Signaling Pathway ◽

Cardiac Fibrosis ◽

Pressure Overload ◽

Akt Signaling ◽

Akt Signaling Pathway

T-cell infiltration and the subsequent increased intracardial chronic inflammation play crucial roles in the development of cardiac hypertrophy and heart failure (HF). A77 1726, the active metabolite of leflunomide, has been reported to have powerful anti-inflammatory and T cell-inhibiting properties. However, the effect of A77 1726 on cardiac hypertrophy remains completely unknown. Herein, we found that A77 1726 treatment attenuated pressure overload or angiotensin II (Ang II)-induced cardiac hypertrophy in vivo, as well as agonist-induced hypertrophic response of cardiomyocytes in vitro. In addition, we showed that A77 1726 administration prevented induction of cardiac fibrosis by inhibiting cardiac fibroblast (CF) transformation into myofibroblast. Surprisingly, we found that the protective effect of A77 1726 was not dependent on its T lymphocyte-inhibiting property. A77 1726 suppressed the activation of protein kinase B (AKT) signaling pathway, and overexpression of constitutively active AKT completely abolished A77 1726-mediated cardioprotective effects in vivo and in vitro. Pretreatment with siRNA targetting Fyn (si Fyn) blunted the protective effect elicited by A77 1726 in vitro. More importantly, A77 1726 was capable of blocking pre-established cardiac hypertrophy in mice. In conclusion, A77 1726 attenuated cardiac hypertrophy and cardiac fibrosis via inhibiting FYN/AKT signaling pathway.

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Leptin receptor expression and its association with PI3K/AKT signaling pathway in diffuse large B-cell lymphoma

Leukemia & Lymphoma ◽

10.3109/10428191003802365 ◽

2010 ◽

Vol 51 (7) ◽

pp. 1305-1314 ◽

Cited By ~ 34

Author(s):

Shahab Uddin ◽

Rong Bu ◽

Maqbool Ahmed ◽

Azhar R. Hussain ◽

Dahish Ajarim ◽

...

Keyword(s):

B Cell ◽

Signaling Pathway ◽

Leptin Receptor ◽

Cell Lymphoma ◽

B Cell Lymphoma ◽

Akt Signaling ◽

Receptor Expression ◽

Akt Signaling Pathway ◽

Large B Cell Lymphoma ◽

Large B Cell

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Identification of biomarkers associated with ovarian cancer based on transcriptome sequencing

10.1101/728618 ◽

2019 ◽

Author(s):

jiazhou chen ◽

xiandong peng ◽

min yu

Keyword(s):

Ovarian Cancer ◽

Cell Adhesion ◽

Western Blot ◽

Signaling Pathway ◽

Transcriptome Sequencing ◽

Akt Signaling ◽

Serous Carcinoma ◽

Receptor Interaction ◽

List Type ◽

Akt Signaling Pathway

AbstractObjectiveThis study aimed to explore more biomarkers associated with ovarian cancer.MethodsCell lines SKOV-3 (ovarian serous carcinoma cells) and MCV152 (benign ovarian epithelial tumor cell) were used in this study and performed transcriptome sequencing. The differentially expressed genes (DEGs) between ovarian cancer cells (SKOV-3) and controls (MCV152) were identified, followed by function enrichment analysis. The expression levels of genes involved in the key pathway were validated through PCR and western blot analyses.ResultsTotal 2,020 upregulated and 1,673 downregulated DEGs were obtained between SKOV3 and MCV152 cells. The upregulated and downregulated DEGs were significantly associated with cell adhesion. In addition, the upregulated DEGs were significantly involved in pathways of ECM-receptor interaction, and the downregulated DEGs were involved in PI3K-Akt signaling pathway. PCR and western blot analyses showed that genes (proteins) expression related to PI3K-Akt signaling pathway were in consistent with bioinformatics analysis.ConclusionCell adhesion and extracellular matrix (ECM)-receptor interaction may play an important role in the invasion of ovarian cancer. PI3K-Akt signaling pathway may be involved in the progression of ovarian cancer by up-regulating ANGPT2, FGF18, ITGB4 and ITGB8, and downregulating AKT3 and PIK3AP1.HighlightsCell adhesion and ECM-receptor interaction may play important roles in ovarian cancer invasion.PI3K-Akt signaling pathway may involve in ovarian cancer progression.ANGPT2, FGF18, ITGB4, ITGB8, AKT3 and PIK3AP1 may serve as biomarkers in ovarian cancer.

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Antioxidant Activity and the Potential Mechanism of the Fruit From Ailanthus altissima Swingle

Frontiers in Veterinary Science ◽

10.3389/fvets.2021.784898 ◽

2021 ◽

Vol 8 ◽

Author(s):

Ya-nan Mo ◽

Feng Cheng ◽

Zhen Yang ◽

Xiao-fei Shang ◽

Jian-ping Liang ◽

...

Keyword(s):

Oxidative Stress ◽

Antioxidant Activity ◽

Signaling Pathway ◽

Radical Scavenging ◽

Akt Signaling ◽

Sirtuin 1 ◽

Ailanthus Altissima ◽

Pathway Enrichment Analysis ◽

Potential Mechanism ◽

Akt Signaling Pathway

The fruits of Ailanthus altissima Swingle (AS) possess a variety of pharmacological activities. Its antioxidant activity and the potential mode of action have not yet been investigated. In in vitro studies, AS revealed the strong reducing power and DPPH scavenging effect, but hydroxyl radical scavenging activity and ferrous ions-chelating ability were not strong. Meanwhile, the oxidative stress RAW264.7 cell injury model was established, the low and medium-doses of AS showed significant protective effects on the viability of H2O2-treated cells by CCK-8 method. Besides, three doses of AS all increased the activities of SOD, CAT, and GSH-Px and decreased the MDA level compared with the H2O2 group, suggesting it significantly relieved oxidative stress of cells. The active ingredients and related targets of AS were collected by HERB and Swiss Target Prediction database, the common targets of drugs and diseases database were conducted by GeneCards database platform and the Venny platform. We screened the core targets of AS like threonine kinase1 (AKT1), mitogen-activated protein kinase 1 (MAPK1), sirtuin-1 (SIRT1), mechanistic target of rapamycin kinase (MTOR) by STRING database, and the key pathways involved PI3K-AKT and FoxO signaling pathway by KEGG pathway enrichment analysis. Besides, qRT-PCR revealed AS preconditioning significantly up-regulated the expression level of AKT1, SIRT1, MAPK1, and MTOR in model cells, and the effect was related to the regulation of FoxO and PI3K/AKT signaling pathway. In summary, AS showed significant antioxidant activity and its potential mechanism was regulating FoxO and PI3K/AKT signaling pathway.

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Identifying hub genes associated with clinical characteristicsin IgA nephropathy by Weighted Gene Co-expression Network Analysis

10.21203/rs.2.15823/v1 ◽

2019 ◽

Author(s):

Chengyu Yang ◽

Chenyu Li ◽

Long Zhao ◽

Bin Zhou ◽

Xiaofei Man ◽

...

Keyword(s):

Iga Nephropathy ◽

Signaling Pathway ◽

Clinical Characteristics ◽

Enrichment Analysis ◽

Akt Signaling ◽

Differentially Expressed ◽

Akt Signaling Pathway ◽

Hub Genes ◽

Renal Interstitium ◽

Healthy Control

Abstract Background: Clinically, IgA nephropathy has a variety of symptoms including paroxysmal gross hematuria, nephritic and nephrotic syndrome. This study aimed at investigating hub geneand genes modular related to IgA nephropathy clinical characteristics by using weighted gene co-expression network analysis combining clinical, microarray and network database parameters. Methods: We collected 32 human samples from the European Renal cDNA Bank and used RMA method to preprocess the data and utilize the limma package to obtain differentially expressed gene in renal interstitium and glomeruli. We used the WGCNA package to construct the gene co-expression of differential expression genes and identify hub genes associated with clinical characteristics in renal interstitium and glomeruli, respectively. Gene ontology enrichment analysis and KEGG analysis for hub genes which associated with clinical characteristics were performed by DAVID. PPI information was acquired from STRING. Results: For glomeruli, 1470 genes differentially expressed between IgA nephropathy patients and healthy control, containing 10 hub genes associated with age, 8 hub genes associated with sex, 48 hub genes associated with Bp enrichd in ERK1 and ERK2 cascade and Rap1 signaling pathway, 223 hub genes associated with BMI enrich in organic acid catabolic process and fatty acid degradation pathway, 136 hub genes associated GFR enriched in immune response and PI3K-Akt signaling pathway, 82 hub genes associated with proteinuria enriched in extracellular matrix organization and PI3K-Akt signaling pathway. In tubulointerstitium, there were 480 genes differentially expressed between IgA nephropathy patients and healthy control. Among 480 DEGs, 6 hub genes associated with age, 15 hub genes associated with sex, 35 hub genes associated with Bp enrichd in positive regulation of apoptotic process, 87 hub genes associated with GFR enriched in negative regulation of macromolecule metabolic process and RNA transport, 33 hub genes associated with proteinuria enriched in regulation of apoptotic process and FoxO signaling pathway. PPI enrichment analysis shown that all hub genes sets are biologically connected cluster. Conclusions: We made a preliminary investigation on molecular mechanisms of relationship between IgA nephropathy and clinical characteristics and identified hub genes and pathways closely related with BMI, GFR and Proteinuria in IgA nephropathy by a series of bioinformatics analysis.

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