Biomechanics and Oxidative Stress: An Integrative Review of the Redox–Mechanobiological Axis and the Role of Trace Elements in Disease

Oxidative stress and mechanobiological signaling are increasingly recognized as interconnected determinants of cellular and systemic homeostasis. Reactive oxygen species (ROS), traditionally associated with molecular damage, are now understood to directly regulate cytoskeletal remodeling, membrane viscoelasticity, mitochondrial dynamics, and mechanotransduction pathways including focal adhesion kinase (FAK), integrins, and Yes-associated protein/transcriptional coactivator with PDZ-binding motif (YAP/TAZ). Conversely, biomechanical forces such as extracellular matrix stiffness, cyclic stretch, and disturbed shear stress modulate intracellular redox signaling through mitochondrial dysfunction, NADPH oxidase activation, and inflammatory pathways. This bidirectional interaction forms a self-amplifying "redox-mechanobiological axis" that contributes to endothelial dysfunction, fibrosis, thrombosis, tumor progression, and viral pathophysiology.Trace elements, particularly selenium, zinc, and iron, emerge as critical modulators of this axis by influencing antioxidant defense systems, cytoskeletal integrity, membrane stability, ferroptosis, and cellular stiffness. Selenium-dependent selenoproteins regulate mitochondrial redox balance and actin organization; zinc stabilizes membrane architecture and mechanosensitive proteins; and iron-mediated Fenton chemistry promotes oxidative injury, ferroptosis, and biomechanical alterations.This review integrates molecular mechanisms, mechanobiological principles, and recent clinical findings-particularly from cardiovascular disease, cancer biology, and COVID-19-to propose a unified framework linking oxidative stress to biomechanical dysfunction. In addition, current controversies, methodological limitations, and future therapeutic directions targeting the redox-mechanobiological axis are critically discussed.