The maintenance of physiological homeostasis is a crucial player for healthy living. Oxidative stress and inflammation are tightly linked biological processes that play central roles in maintaining this balance. Oxidative stress is a consequence of an imbalance between reactive species (ROS/RNS) production and the body’s antioxidant defense systems, leading to oxidative damage to body macromolecules, including lipids, proteins, and DNA. On the other hand, inflammatory responses are initiated through pattern recognition receptors (PRRs) that detect pathogenic and damage-associated signals, activating signaling pathways including NF-κB and MAPK pathways. Emerging evidence describes a bidirectional relationship in which excessive ROS amplifies inflammatory signaling, while activated immune cells further enhance oxidative stress, creating a self-perpetuating cycle. Key signaling molecules, such as HMGB1 and the NLRP3 inflammasome, mediate redox imbalance to cytokine production and immune activation. The oxidative stress-inflammation nexus is a major contributor to the pathophysiology of various disorders, including cardiovascular, neurodegenerative, and metabolic diseases. Therapeutic intervention designed to target this interplay may represent a promising strategy for the treatment of diseases associated with oxidative stress-linked inflammatory responses