Thrombosis research · 2025
Platelet Thromboxane B2 overproduction associated with liver fibrosis severity in patients with MASLD.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Baratta Francesco, Cocomello Nicholas, Carpino Guido, Colantoni Alessandra, Cammisotto Vittoria, Bartimoccia Simona, Castellani Valentina, Overi Diletta, Lucatelli Pierleone, Ettorre Evaristo, Carnevale Roberto, Pignatelli Pasquale, Pastori Daniele, Del Ben Maria, Gaudio Eugenio, Desideri Giovambattista, Violi Francesco
Аннотация
BACKGROUND AND AIMS: Experimental study demonstrated that platelet cyclooxygenase-1 (COX-1) activation is implicated in the pathogenesis of metabolic dysfunction-associated steatosis liver disease (MASLD). However, the relationship between COX-1 activation and MASLD severity is still unclear. This study aimed to investigate platelet COX-1 activation in patients with MASLD.
METHODS: This is a cross-sectional study involving patients with biopsy-proven MASLD. Serum Thromboxane B2 (TxB2) levels was measured as a biomarker of ex vivo COX-1 activation potential and plasma sP-selectin as in vivo marker of platelet activation. Oxidative stress biomarkers included serum NOX2-derived peptide (sNOX2-dp) and hydrogen peroxide breakdown activity (HBA).
RESULTS: TxB2 serum levels increased progressively from MASLD simple steatosis (MASLD-SS) to steatohepatitis (MASH) (p = 0.017) and cirrhosis (p = 0.012). Serum TxB2 (rS = 0.467, p < 0.001) and sNOX2-dp (rS = 0.476, p < 0.001) levels were positively correlated with fibrosis stage and inversely correlated with HBA (rS = -0.506, p < 0.001). In addition, serum TxB2 correlated with sP-selectin (rS = 0.428, p < 0.001). Multivariate linear regression analysis revealed that TxB2 associated with liver fibrosis stage (p = 0.007) and sNOX2-dp (p = 0.018).
CONCLUSIONS: This study provides evidence of platelet TxB2 overproduction, which increases progressively from MASLD-SS to MASH and cirrhosis and is significantly associated with the degree of liver fibrosis. These findings support the hypothesis that platelet COX-1 activation is involved in the pathogenesis of MASLD.
METHODS: This is a cross-sectional study involving patients with biopsy-proven MASLD. Serum Thromboxane B2 (TxB2) levels was measured as a biomarker of ex vivo COX-1 activation potential and plasma sP-selectin as in vivo marker of platelet activation. Oxidative stress biomarkers included serum NOX2-derived peptide (sNOX2-dp) and hydrogen peroxide breakdown activity (HBA).
RESULTS: TxB2 serum levels increased progressively from MASLD simple steatosis (MASLD-SS) to steatohepatitis (MASH) (p = 0.017) and cirrhosis (p = 0.012). Serum TxB2 (rS = 0.467, p < 0.001) and sNOX2-dp (rS = 0.476, p < 0.001) levels were positively correlated with fibrosis stage and inversely correlated with HBA (rS = -0.506, p < 0.001). In addition, serum TxB2 correlated with sP-selectin (rS = 0.428, p < 0.001). Multivariate linear regression analysis revealed that TxB2 associated with liver fibrosis stage (p = 0.007) and sNOX2-dp (p = 0.018).
CONCLUSIONS: This study provides evidence of platelet TxB2 overproduction, which increases progressively from MASLD-SS to MASH and cirrhosis and is significantly associated with the degree of liver fibrosis. These findings support the hypothesis that platelet COX-1 activation is involved in the pathogenesis of MASLD.