Transforming Metabolic Interference into Homeostatic Recovery: Modifying Hepatic Stellate Cell Energy Dynamics for the Reversal of Liver Fibrosis

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Metabolic reprogramming in hepatic stellate cells (HSCs) is a key factor in liver fibrosis progression, involving complex remodeling of metabolic networks.
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Lactate from glycolysis acts as an epigenetic signal, influencing fibrogenic gene expression in activated HSCs.
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Activated HSCs can transmit fibrotic characteristics to neighboring cells via GLUT1-containing exosomes, demonstrating metabolic crosstalk.
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HSC activation shows stage-specific metabolic vulnerabilities, with distinct metabolic states during early and full activation.
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Future anti-fibrotic strategies should focus on restoring metabolic homeostasis and utilize selective metabolic modulators to reverse HSC activation.

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