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Liver fibrosis is a pathological process caused by a variety of chronic liver diseases. Currently, therapeutic options for liver fibrosis are very limited, highlighting the urgent need to explore new treatment approaches. Epigenetic modifications and epitranscriptomic modifications, as reversible regulatory mechanisms, are involved in the development of liver fibrosis. In recent years, researches in epitranscriptomics and epigenetics have opened new perspectives for understanding the pathogenesis of liver fibrosis. Exploring the epigenetic mechanisms of liver fibrosis may provide valuable insights into the development of new therapies for chronic liver diseases. This review primarily focus on the regulatory mechanisms of N6-methyladenosine (m6A) modification, non-coding RNA, and DNA methylation in organ fibrosis. It discusses the interactions between m6A modification and DNA methylation, as well as between m6A modification and non-coding RNA, providing a reference for understanding the interplay between epitranscriptomics and epigenetics.
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http://dx.doi.org/10.1016/j.cellsig.2024.111302 | DOI Listing |
Med Sci (Paris)
September 2025
Service des maladies de l'appareil digestif. Centre de compétence Maladies rares « Maladies inflammatoires des voies biliaires et hépatites autoimmunes », Hôpital Huriez, Lille, France.
Primary biliary cholangitis (PBC) is a rare disease for which management long consisted of a single treatment: ursodeoxycholic acid. In 2015-2016, this disease regained interest with the first studies on obeticholic acid (FXR agonist) and then on bezafibrate (PPAR agonist). Subsequently, over the past five years, significant progress has been made in the management of PBC.
View Article and Find Full Text PDFBackground: Acute kidney injury (AKI) in patients with liver cirrhosis represents a significant clinical challenge with high mortality rates. This study aimed to develop and validate a machine learning-based prediction model for 28-day mortality in AKI patients with liver cirrhosis using the MIMIC-IV database.
Methods: This retrospective study analyzed data from 4,168 AKI patients, including 601 with concurrent liver cirrhosis, from the MIMIC-IV database.
Cell Mol Life Sci
September 2025
Department of Gastroenterology, The Second Hospital of Shandong University, Jinan, China.
Metabolic associated steatohepatitis (MASH) is a severe form of metabolic dysfunction-associated steatotic liver disease (MASLD) characterized by hepatocellular injury, inflammation, and fibrosis. Despite advances in understanding its pathophysiology, the molecular mechanisms driving MASH progression remain unclear. This study investigates the role of long non-coding RNA Linc01271 in MASLD/MASH pathogenesis, ant its involvement in the miR-149-3p/RAB35 axis and PI3K/AKT/mTOR signaling pathway.
View Article and Find Full Text PDFJ Viral Hepat
October 2025
Technion Israel Institute of Technology, Rappaport Faculty of Medicine, Haifa, Israel.
The coexistence of chronic hepatitis B (CHB) and metabolic dysfunction-associated liver disease (MASLD) gained recognition, but the diagnostic performance of non-invasive markers regarding it remains underexplored. This study aimed to evaluate the utility of the FIB-4 index for fibrosis prediction in CHB patients and investigate its performance in the distinct subgroup of CHB-MASLD. A prospective study from 2021 to 2022 included 109 CHB and 64 CHB-MASLD patients.
View Article and Find Full Text PDFLiver Int
October 2025
The Global NASH Council, Washington, DC, USA.
Background: The Middle East and North Africa (MENA) region is undergoing demographic shifts potentially increasing metabolic dysfunction-associated steatotic liver disease (MASLD) and its complications. We assessed MASLD prevalence and liver disease burden from 2010 to 2021.
Methods: Data from Global Burden of Disease (GBD), United Nations Population Division and NCD Risk Factor Collaboration covering 21 MENA countries were used for annual percent change (APC) trends per Joinpoint regression.