Metabolites involved in ACLF progression

Metabolites involved in ACLF progression refers to a diverse set of endogenous small molecules, including intermediates from glucose, amino acid, lipid, and mitochondrial metabolic pathways, which undergo profound quantitative and qualitative changes during acute-on-chronic liver failure. These alterations reflect and drive underlying immune dysfunction, systemic inflammation, energy deficits, and organ failure states characteristic of ACLF. Metabolomics research has identified specific pathways (such as the kynurenine pathway, glycolysis, TCA cycle, pentose phosphate pathway, and amino acid catabolism) and individual metabolites whose dysregulation track with disease severity, prognosis, and (possibly) therapeutic response. However, "metabolites involved in ACLF progression" is not a single molecular entity but a descriptive umbrella term for a set of dynamic metabolic alterations with both biomarker and mechanistic implications in ACLF.

Other names

ACLF-related metabolitesMetabolic biomarkers in ACLFMetabolite signatures in ACLF progression

Modulation of specific metabolic pathways (e.g., inhibition of glycolysis, pentose phosphate pathway, mitochondrial support) Exogenous supplementation or inhibition of pathway metabolites (e.g., replenishment of TCA cycle intermediates or inhibition of kynurenine pathway)