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Moreover, albumin interferes with hemostasis inhibiting platelet aggregation and promoting vasodilation,17 for example through NO-albumin complexes.18 It may also play a role in acid-base homeostasis: on one hand, it behaves as a weak acid and, on the other hand, it can buffer non-volatile acids.19 Lastly, studies in animal models of liver cirrhosis, also found that albumin exerts a positive cardiac inotropic effect counteracting the oxidative stress and TNF- effect in NFB-NOS pathway and b-receptor signalling.55 Forms of Albumin in Liver Cirrhosis Albumin can undergo several posttranslational modifications (PTM) under physiological or pathological conditions, such as oxidation,56,57 glycosylation,5860 truncation at the C- or N-terminus,61,62 dimerization63 and carboxylation.64,65 These PTM result in important structural and functional heterogeneity of circulating albumin.66 Oxidation of cysteine-34 residue is the most frequent PTM in albumin, and is a result of oxidative-stress induced protein damage.62 In healthy subjects, 7080% of albumin circulates in its reduced form, dubbed mercaptoalbumin (HMA), which has a free sulfidril group at cysteine-34.1115 Up to 25% of circulating albumin suffers reversible oxidative modifications through reversible binding via mixed disulfide bridges between cysteine-34 and compounds containing sulfidril groups such as cysteine, homocysteine and glutathione

doi: 10.1096/fj.201601156R 50 FuruyaS.MitomaJ.MakinoA.HirabayashiY

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342 However, its side effects, such as transient thrombocytopenia and neutropenia, remain obstacles to clinical translation