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While T3 and T4 primarily act on hepatocytes to regulate lipid metabolism, THR expression in HSCs suggests that excessive TH levels may activate these cells, potentially contributing to fibrogenesis in hyperthyroid states ( Growing evidence from clinical and experimental studies has established a significant association between hypothyroidismboth overt and subclinicaland the development and progression of MAFLD in both adult and pediatric populations ( 4 )induced liver injury, exogenous TH administration reduced the expression of key fibrogenic genes such as Col1a1 and Col1a2 ( Preclinical and clinical studies collectively support a protective role of thyroid hormones in liver homeostasis, underscoring the therapeutic potential of TH analogs in MAFLD management ( 2.2 Pathogenic mechanisms underlying hypothyroidism-associated MAFLD 2.2.1 Simple steatosis: lipid accumulation and impaired lipophagy Hypothyroidism promotes hepatic lipid accumulation through impaired lipid catabolism, enhanced de novo lipogenesis, and defective autophagic clearance of lipid droplets

Barat Baviera, J.M
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