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Molecular Biology of Liver Diseases: Pathogenesis, Diagnostics and Treatment

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Guest Editor
Section of Gastroenterology and Hepatology, Dipartimento Di Promozione Della Salute, University of Palermo, Palermo, Italy
Interests: study of molecular mechanisms involved in MAFLD development and progression in terms of MASH and HCC; evaluation of the effects of compounds and phytonutrient administration, potentially capable of improving the lipid and glucose metabolic profiles, as well as steatosis and hepatic fibrosis, on in vitro models of continuous human hepatoma cell lines (HepG2) and hepatic stellate cells (LX2)
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Guest Editor
Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties, University of Palermo, 90127 Palermo, Italy
Interests: hepatitis; liver; hepatocellular carcinoma; liver diseases; liver cirrhosis; cirrhosis; liver diseases and immunology; liver failure; chronic hepatitis C; apoptosis

Special Issue Information

Dear Colleagues,

Non-alcoholic fatty liver disease (NAFLD), recently renamed metabolic-associated fatty liver disease (MAFLD), is the most prevalent form of chronic liver disease in the world. The pathogenic mechanism of NAFLD is heterogeneous, complex, and multifactorial, involving a combination of genetic and environmental factors, with an unhealthy lifestyle playing a crucial role in its development.

Studying the molecular mechanisms involved in NAFLD pathogenesis is crucial for developing effective prevention and treatment strategies. Indeed, although many drugs are under investigation, no pharmacological therapy has been approved for this condition, and it lacks adequate non-invasive biomarkers. To date, lifestyle changes play a dominant role in clinical practice.

Research on the pathogenetic mechanisms leading to NAFLD has made significant progress in recent years, though it remains unclear. Several molecular pathways have been proposed, and, to date, insulin resistance seems to be pivotal in the pathogenesis of both NAFLD and type 2 diabetes.

This Special Issue, entitled “Molecular Biology of Liver Diseases: Pathogenesis, Diagnostics and Treatment”, welcomes submissions of original research and review articles on the advancements in molecular mechanism discoveries and novel genetic risk factor identification to contribute to novel prevention and therapeutic approaches. 

Dr. Rosaria Maria Pipitone
Dr. Stefania Grimaudo
Guest Editors

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Keywords

  • non-alcoholic fatty liver disease
  • steatosis
  • fibrogenesis
  • hepatocellular carcinoma
  • hepatocytes
  • hepatic stellate cells
  • inflammation
  • oxidative stress
  • efferocytosis
  • apoptosis

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Published Papers (1 paper)

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Research

15 pages, 7222 KiB  
Article
Linking Antibodies Against Apolipoprotein A-1 to Metabolic Dysfunction-Associated Steatohepatitis in Mice
by Sabrina Pagano, Emmanuel Somm, Catherine Juillard, Nicolas Liaudet, Frédérique Ino, Johan Ferrari, Vincent Braunersreuther, François R. Jornayvaz and Nicolas Vuilleumier
Int. J. Mol. Sci. 2024, 25(22), 11875; https://doi.org/10.3390/ijms252211875 - 5 Nov 2024
Viewed by 1167
Abstract
Metabolic dysfunction-associated fatty liver disease (MASLD) is a common liver and health issue associated with heightened cardiovascular disease (CVD) risk, with Cytokeratin 18 (CK-18) as a marker of liver injury across the MASLD to cirrhosis spectrum. Autoantibodies against apolipoprotein A-1 (AAA-1s) predict increased [...] Read more.
Metabolic dysfunction-associated fatty liver disease (MASLD) is a common liver and health issue associated with heightened cardiovascular disease (CVD) risk, with Cytokeratin 18 (CK-18) as a marker of liver injury across the MASLD to cirrhosis spectrum. Autoantibodies against apolipoprotein A-1 (AAA-1s) predict increased CVD risk, promoting atherosclerosis and liver steatosis in apoE−/− mice, though their impact on liver inflammation and fibrosis remains unclear. This study examined AAA-1s’ impact on low-grade inflammation, liver steatosis, and fibrosis using a MASLD mouse model exposed to AAA-1s passive immunization (PI). Ten-week-old male C57BL/6J mice under a high-fat diet underwent PI with AAA-1s or control antibodies for ten days. Compared to controls, AAA-1-immunized mice showed higher plasma CK-18 (5.3 vs. 2.1 pg/mL, p = 0.031), IL-6 (13 vs. 6.9 pg/mL, p = 0.035), IL-10 (27.3 vs. 9.8 pg/mL, p = 0.007), TNF-α (32.1 vs. 24.2 pg/mL, p = 0.032), and liver steatosis (93.4% vs. 73.8%, p = 0.007). Transcriptomic analyses revealed hepatic upregulation of pro-fibrotic mRNAs in AAA-1-recipient mice, though histological changes were absent. In conclusion, short-term AAA-1 PI exacerbated liver steatosis, inflammation, and pro-fibrotic gene expression, suggesting that AAA-1s may play a role in MASLD progression. Further research with prolonged AAA-1 exposure is warranted to clarify their potential role in liver fibrosis and associated complications. Full article
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