Spermidine‐Based Carbon Quantum Dots Alleviate Liver Sinusoidal Endothelial Dysfunction by Inducing LSEC‐Derived NO to Ameliorate Hepatic Fibrosis and Portal Hypertension

-induced PHT rat models, intravenous ST-CQDs reduced portal pressure by decreasing intrahepatic vascular resistance, reversed LSEC capillarization, inhibited hepatic stellate cell activation and liver fibrosis, and alleviated liver inflammation-without altering systemic hemodynamics or causing organ toxicity. In vitro, ST-CQDs reversed lipopolysaccharide-induced LSEC dysfunction by restoring eNOS expression and NO release. These findings demonstrate ST-CQDs as a potential therapeutic agent for PHT via targeting LSEC-derived NO signaling.