miR-204-5p and miR-130a-3p in Focus: Computational Breakthroughs in Understanding Hypertension Pathogenesis
DOI:
https://doi.org/10.33003/sajols-2024-0204-14Keywords:
Aldosterone; Hypertension; miRNA; Genes; Pathways; TherapeuticsAbstract
Hypertension is a multifactorial disorder influenced by complex genetic and epigenetic interactions. Recent advancements in understanding the role of microRNAs (miRNAs) in regulating gene expression have provided new insights into the molecular mechanisms underlying hypertension. This study investigates the involvement of miRNAs in the pathophysiology of hypertension by analyzing gene expression profiles derived from multiple datasets obtained from NCBI and analyzed with GEOR. miR-DEGs were identified and subjected to the DAVID online tool for gene ontology study. BiBiServ2 was queried for miRNA/mRNA homology study. A total of 1,014 overlapping differentially expressed genes (DEGs) were identified across three datasets, revealing a significant dysregulation of the hypertensive transcriptome. The study further highlights the role of miRNAs, such as miR-29a-3p, miR-204-5p, miR-130a-3p, and miR-145-5p, in targeting these DEGs, with a predominant suppression of gene expression observed in hypertensive conditions. Functional enrichment analysis of miRNA-targeted DEGs revealed significant associations with key pathways involved in vascular remodeling, inflammation, and aldosterone regulation, including MAPK signaling, PI3K-Akt signaling, and the renin-angiotensin-aldosterone system (RAAS). Additionally, miRNA/gene homology studies demonstrated strong binding affinities between these miRNAs and genes involved in aldosterone synthesis, suggesting their pivotal role in modulating blood pressure regulation. The findings underscore the critical involvement of miRNAs in hypertension, proposing their potential as biomarkers and therapeutic targets for hypertension management. Future research should focus on validating these miRNA-targeted pathways and exploring miRNA-based therapeutics to restore homeostasis in hypertension.