Mecanismos de regulação cardiometabólica induzidos pelo exercício físico na prevenção da aterosclerose: uma análise in silico

Abstract

Atherosclerosis is a chronic, multifactorial inflammatory pathology and a leading cause of global mortality, necessitating the investigation of robust preventive strategies. This study aimed to investigate, through bioinformatics and systems biology approaches, the molecular mechanisms by which physical exercise modulates cardiometabolic pathways and prevents disease progression. The methodology consisted of quantitative and descriptive in silico research, based on cross-referencing transcriptomic data from the Fitnoma catalog with the atherosclerosis pathway from the KEGG database, followed by the construction of Protein-Protein Interaction (PPI) networks via the STRING platform and functional enrichment analysis using WebGestalt. The results identified 42 common genes, revealing a molecular network with remarkably high connectivity. The PLCG1 gene emerged as the primary hub involved in calcium signaling and eNOS enzyme activation—processes essential for maintaining vascular homeostasis. Furthermore, critical axes for cell survival (PI3K-AKT) and inflammatory modulation (TLR4-MAPK) were identified. Enrichment analysis highlighted immune system regulation as the central biological process mediated by exercise. In conclusion, physical activity exerts a systemic cardioprotective impact by acting as a coordinated biological cluster that mitigates systemic inflammation, reverses cellular damage, and stabilizes atherosclerotic plaques through gene transcription modulation. These findings validate the use of computational tools for discovering therapeutic