Superoxide Dismutase (SOD) is an antioxidant enzyme that catalyzes the dismutation of superoxide radicals into oxygen and hydrogen peroxide, thus mitigating oxidative stress. Oxidative stress is a known contributing factor in the pathogenesis of various fibrotic diseases, including pulmonary, hepatic, and cardiac fibrosis. Experimental models have demonstrated that SOD administration or overexpression can reduce oxidative damage and attenuate fibrotic progression. For instance, animal studies in pulmonary fibrosis (such as those induced by bleomycin) have shown that SOD mimetics or gene therapies that enhance SOD activity can reduce fibrotic markers and improve tissue histology.

However, direct clinical evidence in humans is limited. Most of the supportive data come from preclinical research using animal models or cellular systems. There are few, if any, large-scale human clinical trials specifically investigating SOD supplementation as a treatment for fibrosis. Additionally, issues such as the delivery and bioavailability of exogenous SOD complicate its practical use in clinical settings. Some research has explored SOD mimetics or gene transfer strategies to overcome these limitations, but these approaches remain largely experimental.

In summary, while there is a scientific rationale and preclinical evidence supporting the role of SOD in reducing fibrosis due to its antioxidant effects, robust human data are lacking. Thus, its use for fibrosis is supported by limited scientific evidence, and more clinical research is needed to establish efficacy and safety.