Review explores oxidative stress and redox biology in tendon injury and repair mechanisms

Tendon injuries are increasingly recognized as conditions driven not only by mechanical overload but also by complex molecular imbalances, particularly involving oxidative stress. Recent evidence highlights the central role of reactive oxygen species (ROS), originating primarily from mitochondrial respiration and NADPH oxidase activation, in regulating cellular responses during tendon injury and repair. Mechanical loading and calcium signaling further influence ROS dynamics, exacerbating oxidative damage or modulating adaptive responses depending on context. Tendon cells counteract oxidative insults through a coordinated antioxidant defense network, including superoxide dismutases, catalase, glutathione peroxidases, and peroxiredoxins. However, in pathological states such as tendinopathy or diabetes, this redox balance is often disrupted, leading to sustained inflammation, extracellular matrix degradation, and impaired healing. This review synthesizes current findings on ROS generation, redox-sensitive signaling pathways, and the functional consequences of oxidative stress in tendon biology. Furthermore, it explores therapeutic strategies targeting redox imbalance, including pharmacological antioxidants and bioengineered scaffolds with antioxidant properties. Understanding these mechanisms provides critical insights into tendon pathophysiology and highlights promising avenues for redox-based regenerative therapies.