Unraveling the Anemia Nexus: Bioinformatics-Driven Discovery of Key Protein Interactions and Therapeutic Targets

Abstract

Anemia, characterized by a deficiency in red blood cells or their oxygen-carrying capacity, is a prevalent condition with significant health impacts. This study utilizes a bioinformatics approach to identify key proteins involved in anemia, leveraging multiple centrality metrics within the anemia protein interaction network to uncover potential therapeutic targets. By analyzing genomic and proteomic data, we identified critical proteins using centrality metrics, including Degree, Closeness, Betweenness, and Radiality. The study focused on five key proteins: GAPDH, EEF2, TPI1, ACO1, and RPS13. These proteins were assessed for their roles in cellular processes related to anemia. Our findings highlight GAPDH's multifunctional roles in glycolysis and iron homeostasis, EEF2's regulation of protein synthesis under stress, TPI1's crucial function in glycolysis and its link to hemolytic anemia, ACO1's dual role in the TCA cycle and iron regulation, and RPS13's importance in protein synthesis and erythropoiesis. Each protein was identified as a significant node within the network, indicating its potential as a biomarker and therapeutic target. The integration of genomic, proteomic, and clinical data revealed that these proteins play pivotal roles in the molecular mechanisms underlying anemia. GAPDH interacts with iron-regulatory proteins, EEF2 modulates protein synthesis, TPI1 mutations lead to hemolytic anemia, ACO1 regulates iron homeostasis and is linked to sideroblastic anemia, and RPS13 contributes to erythropoiesis. This study explores how specific proteins may contribute to the development and progression of anemia. Rather than reinforcing existing models, it introduces fresh biological clues that could reshape how clinicians interpret and treat this condition. These findings point toward personalized treatment options and offer a more refined lens for evaluating patient needs.