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TUDCA could act as a molecular chaperone to ameliorate ER stress and preventing UPR dysfunction in ER stress related diseases such as hepatobiliary disorders, diabetes and obesity [179]

The interplay between HAS3-mediated HA synthesis and HYAL1-driven degradation further exemplifies intrinsic temporal control of ECM remodeling, providing a natural biological model that parallels HAGSH scaffold responsiveness [19]

In the blend, it represents a protein functional component that complements creatine, glutathione, vitamins, and plant-based omega-3 ALA
