7 results match your criteria: "Roger Williams Institute of Liver Studies[Affiliation]"

Soluble Herpes Virus Entry Mediator and Type II/III Interferons Are Upregulated in Primary Biliary Cholangitis.

Int J Mol Sci

January 2025

The Roger Williams Institute of Liver Studies, School of Immunology and Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London & Foundation for Liver Research, London SE5 9NT, UK.

Bacterial translocation-induced inflammation and immune dysfunction are recognised factors contributing to the pathogenesis of primary biliary cholangitis (PBC). However, the specific involvement of interferons (IFNs) and soluble checkpoints (sol-CRs) in shaping the immune landscape in PBC patients remains unexplored. Furthermore, the influence of ursodeoxycholic acid (UDC) on these immune mediators is unknown.

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Background: Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) encompasses a spectrum of histological conditions ranging from simple steatosis to fibrosing steatohepatitis, and is a risk factor for cardiovascular diseases (CVD). While oxidised apolipoproteins A and B have been linked to obesity and CVD, the association between other oxidised apolipoproteins and MASLD is yet to be established. To fill this gap, we characterised the circulating serum peptidome of patients with MASLD.

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Steatotic liver disease (SLD) and Hepatocellular Carcinoma (HCC) are characterised by a substantial rewiring of lipid fluxes caused by systemic metabolic unbalances and/or disrupted intracellular metabolic pathways. SLD is a direct consequence of the interaction between genetic predisposition and a chronic positive energy balance affecting whole-body energy homeostasis and the function of metabolically-competent organs. In this review, we discuss how the impairment of the cross-talk between peripheral organs and the liver stalls glucose and lipid metabolism, leading to unbalances in hepatic lipid fluxes that promote hepatic fat accumulation.

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Oral-gut microbiome interactions in advanced cirrhosis: characterisation of pathogenic enterotypes and salivatypes, virulence factors and antimicrobial resistance.

J Hepatol

October 2024

Roger Williams Institute of Liver Studies, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom; Institute of Liver Studies, King's College Hospital NHS Foundation Trust, London, United Kingdom. Electronic address:

Article Synopsis
  • The study investigates how the gut and oral microbiomes are affected in patients with varying severities of cirrhosis, focusing on the presence of harmful bacteria and resistance genes.
  • It involves analysis of samples from multiple groups: healthy controls, stable cirrhosis, decompensated cirrhosis, acute-on-chronic liver failure patients, and those with severe infections but no cirrhosis.
  • Results show increased overlap of oral and gut microbiomes and greater amounts of virulence factors and antibiotic resistance genes as cirrhosis severity increases, suggesting a shift towards more harmful bacteria and a loss of beneficial ones.
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Background: Semaglutide, a glucagon-like peptide-1 receptor agonist, has demonstrated potential beneficial effects in metabolic dysfunction-associated steatohepatitis (MASH).

Aims: To describe the trial design and baseline characteristics of the 'Effect of Semaglutide in Subjects with Non-cirrhotic Non-alcoholic Steatohepatitis' (ESSENCE) trial (NCT04822181).

Methods: ESSENCE is a two-part, phase 3, randomised, multicentre trial evaluating the effect of subcutaneous semaglutide 2.

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Article Synopsis
  • Gremlin-1 has been linked to liver fibrosis in metabolic dysfunction-associated steatohepatitis (MASH) by inhibiting BMP signaling, making it a potential focus for therapy.* -
  • In studies using rat and human models, blocking Gremlin-1 with antibodies did not reduce liver inflammation or fibrosis, despite its increased presence in specific myofibroblast cells.* -
  • Findings indicate that Gremlin-1 does not significantly contribute to liver fibrosis development and is not a viable target for treatment due to its limited role in the disease process.*
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