Shining light on liquid-liquid phase separation in chronic liver disease.

Liquid-liquid phase separation (LLPS), a phenomenon characterized by a membrane-free structure formed by weak multivalent interactions of intracellular biological macromolecules, has attracted wide attention in the study of chronic liver diseases in recent years. LLPS has multiple roles in the occurrence and development of chronic liver disease, including regulating virus replication, affecting lipid metabolism, regulating immune response, and participating in the regulation of gene expression. This article reviews the specific mechanism of LLPS in chronic liver disease, and discusses its potential application in drug development, immunotherapy, and gene therapy, providing new ideas for the treatment of chronic liver disease.

Novel insights on post-translational modifications of nucleic acid methylation proteins in hepatic fibrosis.

Hepatic fibrosis is a pathologic state in which there is an excessive accumulation of the extracellular matrix (ECM) components within the liver parenchyma. It is an ongoing process that compromises the structure and functional performance of the liver tissue. Without treatment, it may progress to end-stage liver disease, including cirrhosis and hepatocellular carcinoma.

Novel epitranscriptomic and epigenetic therapeutic strategies and targets for ferroptosis in liver fibrosis.

Liver fibrosis is characterized by an excessive accumulation of extracellular matrix (ECM) and the activation of hepatic stellate cells (HSCs), which are influenced by epitranscriptomic and epigenetic factors. Recent advancements in epigenetic and epitranscriptomic research have revealed new opportunities for therapeutic interventions, particularly through the regulation of ferroptosis, a type of programmed cell death that is specifically linked to iron-dependent lipid peroxidation. In the context of liver fibrosis, a progressive scarring process that can progress to cirrhosis and ultimately end-stage liver disease, targeting these regulatory mechanisms to modulate ferroptosis presents a promising therapeutic strategy.

Association of NLR with all-cause and cardiovascular mortality in adults with coronary heart disease: 1999-2018 NHANES data analysis.

The neutrophil-to-lymphocyte ratio (NLR) is an important inflammatory marker. However, the relationship between NLR and the prognosis of patients with coronary heart disease (CHD) remains unclear. The purpose of this study is to explore the relationship between NLR and all-cause mortality and cardiovascular mortality in CHD patients.

Epitranscriptomic regulation of lipid oxidation and liver fibrosis via ENPP1 mRNA mA modification.

Background: Dysregulated lipid oxidation occurs in several pathological processes characterized by cell proliferation and migration. Nonetheless, the molecular mechanism of lipid oxidation is not well appreciated in liver fibrosis, which is accompanied by enhanced fibroblast proliferation and migration.

Methods: We investigated the causes and consequences of lipid oxidation in liver fibrosis using cultured cells, animal models, and clinical samples.

m6A epitranscriptomic and epigenetic crosstalk in liver fibrosis: Special emphasis on DNA methylation and non-coding RNAs.

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.

TET3 boosts hepatocyte autophagy and impairs non-alcoholic fatty liver disease by increasing ENPP1 promoter hypomethylation.

Background: Dysregulated ecto-nucleotide pyrophosphatase/phosphodiesterase (ENPP) family occurs in metabolic reprogramming pathological processes. Nonetheless, the epigenetic mechanisms by which ENPP family impacts NAFLD, also known as metabolic dysfunction-associated steatotic liver disease (MASLD), is poorly appreciated.

Methods: We investigated the causes and consequences of ENPP1 promoter hypomethylation may boost NAFLD using NAFLD clinical samples, as well as revealed the underlying mechanisms using high-fat diet (HFD) + carbon tetrachloride (CCl) induced mouse model of NAFLD and FFA treatment of cultured hepatocyte.