Research on GM1 bound bMSCs loaded with SF hydrogel for spinal cord injury repair.

Osteoarthritis (OA) ranks among the most prevalent degenerative joint disorders, imposing a profound and growing clinical and socioeconomic burden worldwide []. Since articular cartilage lacks intrinsic regenerative capacity, structural deterioration of OA is generally considered irreversible. As the disease advances, progressive cartilage loss culminates in impaired joint function and ultimately leads to joint dysfunction or disability []. At present, clinical strategies for OA focus on attenuating inflammation and alleviating pain, which cannot effectively and completely prevent disease progression []. In recent years, increasing studies have implicated that increased levels of various reactive oxygen species (ROS), including •O, •OH, and HO, contribute to an oxidative joint milieu that drives pathological changes [,]. Local oxidative stress within the articular cartilage microenvironment leads to degradation of the extracellular cartilage matrix. Local oxidative stress in the inflammatory joint milieu culminates in catabolism of the cartilage extracellular matrix and synovial inflammation, thereby accelerating disease progression []. The interplay between ROS and cartilage degeneration creates a vicious cycle, impeding cartilage repair and worsening OA symptoms. Hence, the key to OA therapy hinges on neutralizing multiple types of ROS and attenuating the proinflammatory microenvironment. Therapeutic approaches should therefore combine broad-spectrum ROS scavengers with anti-inflammatory interventions to restore joint homeostasis and promote effective long-term cartilage repair. Endogenous antioxidant enzymes, including superoxide dismutase (SOD), constitute a vital component of the human antioxidant defense system []. While the therapeutic potential of exogenous SOD has been demonstrated, its clinical application is hindered by its intrinsic instability and rapid clearance from the human body. Catalytic biomaterials, biocompatible substances engineered to mimic enzyme activities that exhibit enhanced stability and tunability, have opened new frontiers for therapeutic interventions [–]. Recent advances have led to the development of single-atom nanozymes featuring metal–nitrogen coordination motifs to replicate the catalytic functions of natural enzymes [,]. Despite exhibiting potent catalase (CAT)-mimetic ability that supports antioxidant defenses and oxygen generation, these nanozymes fail to scavenge highly reactive •OH within the OA inflammatory milieu []. Consequently, engineering nanozymes with potent broad-spectrum antioxidant functions to eliminate multiple reactive oxygen species simultaneously is essential for effective OA treatment []. Furthermore, the regulatory mechanism through which nanozymes mitigate OA remains to be elucidated.