Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis
By Herbert Tilg, A. Moschen. Hepatology, 2010
2,421 citations recorded by the source corpus.
Subfields: Cell Biology, Endocrinology, Diabetes and Metabolism, Epidemiology
View Paper: https://www.semanticscholar.org/paper/23b5d8d4a676be45c3fbf11b5b3c6e72acddfa6d
How researchers see this paper
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In Cell Biology
In Endocrinology, Diabetes and Metabolism
In Epidemiology
- Christopher D. Byrne
- G. Targher
- Herbert Tilg
- M. Pinzani
- E. Tsochatzis
- Natascha Roehlen
- E. Crouchet
- E. Buzzetti
Citations in the corpus
- Liver Fibrosis: Mechanistic Concepts and Therapeutic Perspectives (2020, background): “HSCs activation by oxidative stress and inflammation plays a leading role in NASH disease progression and fibrosis development [213].”
- NAFLD and increased risk of cardiovascular disease: clinical associations, pathophysiological mechanisms and pharmacological implications (2020, neutral): “44 Various lipid-related pathways may ‘drive’ hepatic inflammatory pathways in NAFLD.”
- Role of Oxidative Stress in Pathophysiology of Nonalcoholic Fatty Liver Disease (2018, background): “This first hypothesis has been subsequently revised in a “multiple parallel-hit”model in which, in the presence of a significant accumulation of fat in hepatocytes and systemic and hepatic insulin resistance, multiple simultaneous alterations lead to an imbalance between the antilipotoxic protection”
- MASLD: a systemic metabolic disorder with cardiovascular and malignant complications (2024, background): “39 These ‘multiple hits’ can activate proinflammatory cascades, including various inflammatory cytokines and inflammasomes, such as the NLR family pyrin domain containing 3 (NLRP3).”
- The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). (2016, background): “Furthermore, enteric bacteria suppress the synthesis of fasting-induced adipocyte factor (Fiaf) resulting in increased lipoprotein lipase activity and increased triglyceride accumulation [51].”