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Additionally, certain medical interventions, particularly cancer immunotherapies using immune-checkpoint inhibitors (ICIs), have been reported to precipitate autoimmune thyroiditis by enhancing T-cellmediated immune responses and breaking self-tolerance (Barroso-Sousa et al

Glucagon receptor activation increases energy expenditure, promotes hepatic fat oxidation, and drives lipolysis

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However, the proatherogenic mechanisms of p53 deficiency cannot yet be explained by a decrease in apoptosis or cellular proliferation