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When lysosomal function is severely impaired, lysosome-independent degradation pathways, such as those activated by Bortezomib, a proteasome modulator, can enhance ubiquitination and proteasomal activity, compensating for defective lysosomal function and facilitating the removal of damaged proteins and organelles, thus improving immunotherapy efficacy (133) ( Table 1 )
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In osteoarthritis research models, the 177-191 fragment has demonstrated the ability to enhance the differentiation of myoblasts into muscle tissue and promote the regeneration of hyaline cartilage, indicating that while it lacks systemic anabolic properties, it retains localized regenerative signaling distinct from its lipolytic capabilities
