Sodium-glucose cotransporter 2 (SGLT2) inhibitors, initially developed for type 2 diabetes, have unexpectedly demonstrated significant anti-fibrotic effects in non-alcoholic steatohepatitis (NASH), presenting a paradigm shift in hepatology. However, the underlying mechanism remains a critical paradox, as SGLT2 expression is nearly absent in the healthy liver parenchyma. Prevailing hypotheses centered on indirect systemic metabolic improvements fail to fully account for the direct and rapid molecular changes observed within the liver. This review aims to bridge this knowledge gap by proposing a novel, unifying hypothesis. We posit that within the pathological microenvironment of liver fibrosis, a profound cellular crosstalk initiates a phenotypic switch in non-parenchymal cells like liver sinusoidal endothelial cells (LSECs) and hepatic stellate cells (HSCs). We propose that pro-inflammatory cytokines (via NF-κB) and the concomitant hypoxic stress (via HIF-1α) collaboratively drive the transcriptional upregulation of SGLT2. This 'metabolic hijacking' occurs in parallel with a HIF-1α-driven shift to glycolysis, creating a state of 'metabolic vulnerability' where cells become exquisitely dependent on this new glucose supply line.Consequently, we argue that SGLT2 inhibitors exert their direct anti-fibrotic effects by exploiting this vulnerability. By blocking this crucial glucose supply, the inhibitors precipitate a severe 'energy crisis' specifically within activated LSECs and HSCs. This acute energy deficit activates the master energy sensor, AMP-activated protein kinase (AMPK), which orchestrates a dual restorative response. AMPK directly enhances endothelial nitric oxide synthase (eNOS) phosphorylation to restore NO bioavailability, while also suppressing HIF-1α in a self-amplifying feedback loop that dismantles the pro-fibrotic metabolic program. This model provides a comprehensive, cell-specific mechanism that integrates inflammation, hypoxia, and metabolic reprogramming to explain the direct and sustained therapeutic action of SGLT2 inhibitors in liver fibrosis.