ArticleLiver international : official journal of the International Association for the Study of the Liver2026
Albumin Restores Endothelial Cell Mitochondrial Morphology in Patients With Decompensated Cirrhosis.
Article in Liver international : official journal of the International Association for the Study of the Liver, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Acute-on-Chronic Liver Failure: An Eroded Cliff Hit by a Storm-A Narrative Review.International journal of molecular sciences · 2026Review
- Beyond the Tipping Point: Advances in the Diagnosis and Management of Acute-on-Chronic Liver Failure and End-Stage Liver Disease.Diagnostics (Basel, Switzerland) · 2026Review
- Albumin Restores Endothelial Cell Mitochondrial Morphology in Patients With Decompensated Cirrhosis.Liver international : official journal of the International Association for the Study of the Liver · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsEndothelial cell (EC) activation is a critical driver of disease progression in cirrhosis, contributing to acute decompensation (AD) and acute-on-chronic liver failure (ACLF). Although human albumin administration improves EC function in cirrhotic patients with hypoalbuminemia, its direct effects on ECs remain unclear. This ex vivo study investigates the impact of albumin on EC morphology and mitochondrial function upon exposure to plasma from patients with decompensated cirrhosis (DC).
methodsHuman umbilical vein ECs were exposed to plasma from patients with DC and hypoalbuminemia (albumin < 30 g/L, n = 20), compensated cirrhosis (CC, > 30 g/L, n = 20), or healthy controls (HC, n = 20). Albumin was added to DC and HC plasma to reach physiological (~40 g/L) or supraphysiological levels. Mitochondrial function was assessed by measuring oxygen consumption rate (OCR) and reactive oxygen species (ROS) production. The effects of albumin on EC activation were tested using circulating factors elevated in DC (lipopolysaccharide (LPS), tumour necrosis factor-α (TNFα), bilirubin).
resultsMitochondrial morphology distinguished ECs exposed to DC plasma from those exposed to CC or HC plasma. Albumin supplementation shifted EC morphology towards a healthier phenotype. ECs exposed to DC plasma showed increased mitochondrial respiration without a concomitant increase in ROS production, which was normalised by albumin. Albumin had no significant effects on EC activation induced by circulating factors.
conclusionsPlasma from patients with DC and hypoalbuminemia induces EC morphological changes, particularly in mitochondria. Albumin mitigates these effects, suggesting a direct modulatory role on mitochondrial function and supporting its therapeutic potential in vascular dysfunction in cirrhosis.
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