Answers are grounded in this paper and cite their sources.
Objective: Immunoglobulin A nephropathy and membranous nephropathy are glomerulus disease. The current study was planned to understand the molecular mechanism of immunoglobulin A nephropathy and membranous nephropathy with discovery of key micro ribonucleic acids and their targeted hub genes. Methods: The microarray dataset was downloaded from Gene Expression Omnibus database and examined through R package Gene Expression Omnibus 2R. Subsequently, the data was analysed to detect the differential expressed genes. The hub genes were detected using bioinformatics analysis techniques, such as protein-protein interaction network analysis, module analysis and micro ribonucleic acid-messenger ribonucleic acid network construction. The study relied entirely on publicly available datasets conducted in 2021 at COMSATS University Islamabad, Sahiwal Campus. Results: A total of 949 differential expressed genes were recognised. All of them were upregulated genes. Afterward, 6 overlapped genes (Fos proto-oncogene AP-1 transcription factor subunit, Signal Transducer and Activator of Transcription 3, Forkhead Box O3, Heat Shock Protein 90 Alpha Family Class A Member 1, Heat Shock Protein Family A [Hsp70] Member 5 and Tumour Protein p53) were intersected from cytoHubba plugin, designated as hub genes. One novel micro ribonucleic acid, has-miR-495-3p, was identified as biomarker for diagnosis and therapy of immunoglobulin A nephropathy and membranous nephropathy. Conclusion: The short, non-coding has-miR-495-3p was found to be proficient in refining personalised diagnosis and treatments for immunoglobulin A nephropathy and membranous nephropathy patients. In vivo and in vitro analyses of micro ribonucleic acids and network interactions may help further explore the processes underlying the disease.
No takes yet. Share an insight, caveat, or question.
Irfan et al. (2026) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: