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Its mechanism involves activating the AMPK/SIRT1 pathways and suppressing lipogenic regulators like PPARγ and SREBP-1c, highlighting its potential as a therapeutic candidate for NAFLD (96)

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In addition, it has been debated whether erythrocyte membrane injury could promote the thrombotic complications frequently observed in COVID-19 patients [342], and that reduced deformability of erythrocytes may contribute to inflammation and hypoxia in COVID-19 patients [343]