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Specific knockout of TXNIP in LSECs leads to sinusoidal capillarisation, reduced NO production and increased inflammation, thereby aggravating liver injury, fibrosis and HCC development in ALD.26 Conversely, overexpression of TXNIP reverses these effects.26 The loss of fenestrae and the capillarisation of LSECs are also associated with disrupted crosstalk between LSECs and other liver cells, including hepatocytes, HSCs and macrophages, further contributing to the development of liver fibrosis.27 Moreover, elevated plasma markers such as vascular cell adhesion molecule-1, intercellular adhesion molecule-1, E-selectin and von Willebrand factor are observed in patients with severe AH and are associated with disease severity and prognosis.28 These endothelial dysfunction markers suggest that LSECs play a critical role in the pathogenesis of ALD and may serve as predictors of patient outcomes in AH