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Abnormal protein folding due to ER dysfunction can trigger cell apoptosis and fibrosis, exacerbating disease progression in TAO ( Understanding the interplay between ER oxidative stress and TAO requires further basic and clinical research to validate these mechanisms and develop targeted therapeutic strategies

There are also many multi-target dual agonists under development, such as GLP-1R/GCGR, GLP-1R/fibroblast growth factor 21 receptor (FGF21R), etc

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