Fig. 8From: Didymin alleviates metabolic dysfunction-associated fatty liver disease (MAFLD) via the stimulation of Sirt1-mediated lipophagy and mitochondrial biogenesisSchematic representation of Didymin alleviates MAFLD through the Sirt1 pathway. Didymin binds to SIRT1 protein and activates its deacetylase activity, which in turn deacetylates FoxO3a and PGC-1α and enhances their activity. FoxO3a further increases the expression level of SIRT1 and promotes the process of lipophagy. The increase in lipophagy activity can further inhibit cell apoptosis. PGC-1α enhances mitochondrial biosynthesis and improves mitochondrial function by promoting the transcription of NRF1 and TFAM. PGC-1α proliferative activated receptor γ coactivator 1α, NRF1 nuclear respiratory factor 1, TFAM mitochondrial transcription factor A, FoxO3a Foxkhead Box Class O 3a, PLIN2 perilipin 2, LAMP1 lysosomal associated membrane protein 1, Bax Bcl-2-associated X protein, Bcl2 B-cell lymphoma 2Back to article page