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Fig. 8 | Journal of Translational Medicine

Fig. 8

From: Didymin alleviates metabolic dysfunction-associated fatty liver disease (MAFLD) via the stimulation of Sirt1-mediated lipophagy and mitochondrial biogenesis

Fig. 8

Schematic 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 2

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