Results 31 to 40 of about 10,125,713 (289)

Enhanced mitochondrial activity reshapes a gut microbiota profile that delays NASH progression

open access: yesHepatology, EarlyView., 2022
Improved mitochondrial activity, due to the lack of methylation‐controlled J protein (MCJ), creates a specific microbiota signature that when transferred through cecal microbiota transplantation delays NASH progression by restoring the gut‐liver axis and enhancing hepatic fatty acid oxidation.
María Juárez‐Fernández   +18 more
wiley   +1 more source

Non-alcoholic steatohepatitis

open access: yesEuropean Journal of Gastroenterology & Hepatology, 2004
Non-alcoholic steatohepatitis (NASH) is an underdiagnosed liver disease characterized by steatosis, necroinflammation and fibrosis. This disease may eventually develop into cirrhosis and hepatocellular carcinoma. NASH is highly prevalent among obese individuals and among patients with diabetes mellitus type 2.
R, Vecchione   +3 more
openaire   +5 more sources

The SOD2 C47T polymorphism influences NAFLD fibrosis severity: evidence from case-control and intra-familial allele association studies. [PDF]

open access: yes, 2011
AIMS: Non-alcoholic fatty liver disease (NAFLD) is a complex disease trait where genetic variations and environment interact to determine disease progression.
Patch, Julia   +32 more
core   +1 more source

Extracellular vesicles in non-alcoholic and alcoholic fatty liver diseases

open access: yesLiver Research, 2018
Fatty liver diseases, non-alcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) are the most common causes of chronic liver diseases around the world.
Akiko Eguchi, Ariel E. Feldstein
doaj   +1 more source

Mitochondrial stress in advanced fibrosis and cirrhosis associated with chronic hepatitis B, chronic hepatitis C, or nonalcoholic steatohepatitis

open access: yesHepatology, EarlyView., 2022
Adaptive mitochondrial mechanisms allow mitochondrial resilience and prevent the worsening of fibrosis, while deregulation of these mechanisms promotes the progression from no/minimal‐mild (F0‐F2) fibrosis to advanced fibrosis and cirrhosis (F3‐F4). Abstract Background and Aims Hepatitis B virus (HBV) infection causes oxidative stress (OS) and alters ...
Dimitri Loureiro   +17 more
wiley   +1 more source

Lifestyle modification in NAFLD/NASH: Facts and figures

open access: yesJHEP Reports, 2019
Summary: The development of non-alcoholic fatty liver disease is closely linked to lifestyle factors, namely excessive caloric intake coupled with reduced physical activity and exercise. This review aims to examine the evidence behind lifestyle change as
Kate Hallsworth, Leon A. Adams
doaj   +1 more source

Janus kinase 2 inhibition by pacritinib as potential therapeutic target for liver fibrosis

open access: yesHepatology, EarlyView., 2022
Diagram of the activation of the profibrotic and procontractile Janus kinase 2 (JAK2)/Ras homolog family member A/Rho‐kinase pathway and the inhibition of phosphorylated JAK2 by pacritinib to inhibit hepatic stellate cell activity. Abstract Background and Aims Janus kinase 2 (JAK2) signaling is increased in human and experimental liver fibrosis with ...
Sandra Torres   +21 more
wiley   +1 more source

Methionine- and choline-deficient diet induces hepatic changes characteristic of non-alcoholic steatohepatitis

open access: yesArquivos de Gastroenterologia, 2011
CONTEXT: Non-alcoholic steatohepatitis is a disease with a high incidence, difficult diagnosis, and as yet no effective treatment. So, the use of experimental models for non-alcoholic steatohepatitis induction and the study of its routes of development ...
Éder Marcolin   +5 more
doaj   +1 more source

Metabolic preconditions for the formation and progression of steatohepatitis of alcoholic, mixed, non-alcoholic aetiology and their comorbidity with obesity and anaemic conditions

open access: yesMìžnarodnij Endokrinologìčnij Žurnal, 2023
Background. The urgency of the problem of comorbidity of alcoholic steatohepatitis (ASH) and non-alcoholic steatohepatitis (NASH) with anaemic conditions and the need for their differentiated correction is determined by the significant frequency of these
T. Antofiichuk   +3 more
doaj   +1 more source

Interleukin‐18 signaling promotes activation of hepatic stellate cells in mouse liver fibrosis

open access: yesHepatology, EarlyView., 2022
Interleukin‐18 signaling promotes activation of hepatic stellate cells in mouse liver fibrosis. Abstract Background and Aims Nucleotide‐binding oligomerization domain‐like receptor‐family pyrin domain‐containing 3 (NLRP3) inflammasome activation has been shown to result in liver fibrosis.
Jana Knorr   +19 more
wiley   +1 more source

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