MPO-DNA Complexes and cf-DNA in Patients with Sepsis and Their Clinical Value.

Neutrophils, as the first line of defense in the immune response, produce neutrophil extracellular traps (NETs) upon activation, which are significant in the pathogenesis and organ damage in sepsis. This study aims to explore the clinical value of myeloperoxidase-DNA (MPO-DNA) and cell-free DNA (cf-DNA) in sepsis patients. Clinical data were collected from 106 sepsis patients, 25 non-sepsis patients, and 51 healthy controls.

Metabolic Dysregulation and Metabolite Imbalances in Acute-on-chronic Liver Failure: Impact on Immune Status.

Liver failure encompasses a range of severe clinical syndromes resulting from the deterioration of liver function, triggered by factors both within and outside the liver. While the definition of acute-on-chronic liver failure (ACLF) may vary by region, it is universally recognized for its association with multiorgan failure, a robust inflammatory response, and high short-term mortality rates. Recent advances in metabolomics have provided insights into energy metabolism and metabolite alterations specific to ACLF.

IDH1/MDH1 deacetylation promotes NETosis by regulating OPA1 and autophagy.

Background: As a heterogeneous and life-threatening disease, the pathogenesis of acute liver failure (ALF) is complex. Our previous study has shown that IDH1/MDH1 deacetylation promotes ALF by regulating NETosis (a novel mode of cell death). In this article, we explore the manners of IDH1/MDH1 deacetylation regulates NETosis.

Deacetylated MDH1 and IDH1 aggravates PANoptosis in acute liver failure through endoplasmic reticulum stress signaling.

Acute liver failure (ALF) is a disease with a high mortality rate and poor prognosis, whose pathogenesis is not fully understood. PANoptosis is a recently proposed mode of cell death characterized by pyroptosis, apoptosis, and necroptosis, but it cannot be explained by any of them alone. This study aims to explore the role of PANoptosis in ALF and the impact and mechanism of deacetylated malate dehydrogenase 1 (MDH1) and isocitrate dehydrogenase 1 (IDH1) on PANoptosis.

[Retracted] HCV‑E2 inhibits hepatocellular carcinoma metastasis by stimulating mast cells to secrete exosomal shuttle microRNAs.

[This retracts the article DOI: 10.3892/ol.2017.

The acetylation of MDH1 and IDH1 is associated with energy metabolism in acute liver failure.

The liver is the main organ associated with metabolism. In our previous studies, we identified that the metabolic enzymes malate dehydrogenase 1 (MDH1) and isocitrate dehydrogenase 1 (IDH1) were differentially expressed in ALF. The aim of this study was to explore the changes in the acetylation of MDH1 and IDH1 and the therapeutic effect of histone deacetylase (HDAC) inhibitor in acute liver failure (ALF).

Self-Oxidated Hydrophilic Chitosan Fibrous Mats for Fatal Hemorrhage Control.

Enriching erythrocytes and platelets in seconds and providing a fast seal in bleeding sites is vital to fatal hemorrhage control. Herein, hydrophilic chitosan fibrous mats (CECS-D mats) are fabricated by introducing hydrophilic carboxyethyl groups and subsequent catechol groups onto chitosan fibers. Due to strong hydrophilicity, CECS-D mats exhibit rapid liquid-absorption capacity, especially instantaneous absorptivity to the rabbit blood, which can achieve erythrocyte and platelet aggregations quickly by concentrating blood, thus promoting the formation of blood clots.

IDH1/MDH1 deacetylation promotes acute liver failure by regulating NETosis.

Background: Acute liver failure (ALF) is a life-threatening disease, but its pathogenesis is not fully understood. NETosis is a novel mode of cell death. Although the formation of neutrophil extracellular traps (NETs) has been found in various liver diseases, the specific mechanism by which NETosis regulates the development of ALF is unclear.

Distinct Types of Cell Death and Implications in Liver Diseases: An Overview of Mechanisms and Application.

Cell death is associated with a variety of liver diseases, and hepatocyte death is a core factor in the occurrence and progression of liver diseases. In recent years, new cell death modes have been identified, and certain biomarkers have been detected in the circulation during various cell death modes that mediate liver injury. In this review, cell death modes associated with liver diseases are summarized, including some cell death modes that have emerged in recent years.

Sulforaphane, an NRF2 agonist, alleviates ferroptosis in acute liver failure by regulating HDAC6 activity.

Objective: Acute liver failure (ALF) is characterized by severe liver dysfunction, rapid progression and high mortality and is difficult to treat. Studies have found that sulforaphane (SFN), a nuclear factor E2-related factor 2 (NRF2) agonist, has anti-inflammatory, antioxidant and anticancer effects, and has certain protective effects on neurodegenerative diseases, cancer and liver fibrosis. This paper aimed to explore the protective effect of SFN in ALF and it possible mechanisms of action.

Inhibition of GSK3β activity alleviates acute liver failure via suppressing multiple programmed cell death.

Background: Acute liver failure (ALF) is one of the most common life-threatening diseases in adults without previous liver disease. Glycogen synthase kinase 3β (GSK3β) is a serine/threonine protein kinase that is widely distributed in the cells. Inhibition of its activity can inhibit cell death and promote autophagy through various pathways, thus providing a protective effect.

PANoptosis: A Cell Death Characterized by Pyroptosis, Apoptosis, and Necroptosis.

PANoptosis is a new cell death proposed by Malireddi et al in 2019, which is characterized by pyroptosis, apoptosis and necroptosis, but cannot be explained by any of them alone. The interaction between pyroptosis, apoptosis and necroptosis is involved in PANoptosis. In this review, from the perspective of PANoptosis, we focus on the relationship between pyroptosis, apoptosis and necroptosis, the key molecules in the process of PANoptosis and the formation of PANoptosome, as well as the role of PANoptosis in diseases.

AGK2 pre-treatment protects against thioacetamide-induced acute liver failure via regulating the MFN2-PERK axis and ferroptosis signaling pathway.

Background: Acute liver failure (ALF) is an unpredictable and life-threatening critical illness. The pathological characteristic of ALF is massive necrosis of hepatocytes and lots of inflammatory cells infiltration which may lead to multiple organ failure.

Methods: Animals were divided into 3 groups, normal, thioacetamide (TAA, ALF model) and TAA + AGK2.

Interventions for non-alcoholic liver disease: a gut microbial metabolites perspective.

Over the past two decades, non-alcoholic fatty liver disease (NAFLD) has become a leading burden of hepatocellular carcinoma and liver transplantation. Although the exact pathogenesis of NAFLD has not been fully elucidated, recent hypotheses placed more emphasis on the crucial role of the gut microbiome and its derivatives. Reportedly, microbial metabolites such as short-chain fatty acids, amino acid metabolites (indole and its derivatives), bile acids (BAs), trimethylamine N-oxide (TMAO), and endogenous ethanol exhibit sophisticated bioactive properties.

NOD2-mediated HDAC6/NF-κb signalling pathway regulates ferroptosis induced by extracellular histone H3 in acute liver failure.

Acute liver failure (ALF) is life-threatening and often associated with high mortality rates. The aim of the present study was to investigate whether extracellular histone H3 could induce ferroptosis in hepatic macrophages in ALF and explore its potential mechanism. RAW264.

SIRT3 inhibitor 3-TYP exacerbates thioacetamide-induced hepatic injury in mice.

The purpose of the study was to explore the effects of SIRT3 inhibitor 3-TYP on acute liver failure (ALF) in mice and its underlying mechanism. The mice were treated with thioacetamide (TAA, 300 mg/kg) for inducing ALF model. 3-TYP (50 mg/kg) was administered 2 h prior to TAA.

Fusobacterium nucleatum promotes the development of acute liver failure by inhibiting the NAD salvage metabolic pathway.

Background: Acute liver failure (ALF) patients are often accompanied by severe energy metabolism abnormalities and intestinal microecological imbalance. The intestinal mucosal barrier is severely damaged. Intestinal endotoxin can induce intestinal endotoxemia through the "Gut-Liver axis".

Sirtuin1 attenuates acute liver failure by reducing reactive oxygen species hypoxia inducible factor 1α.

Background: The occurrence and development of acute liver failure (ALF) is closely related to a series of inflammatory reactions, such as the production of reactive oxygen species (ROS). Hypoxia inducible factor 1α (HIF-1α) is a key factor that regulates oxygen homeostasis and redox, and the stability of HIF-1α is related to the ROS level regulated by Sirtuin (Sirt) family. The activation of Sirt1 will lead to a powerful antioxidant defense system and therapeutic effects in liver disease.

Changes of flavin-containing monooxygenases and trimethylamine-N-oxide may be involved in the promotion of non-alcoholic fatty liver disease by intestinal microbiota metabolite trimethylamine.

Evidence shows that trimethylamine (TMA)/trimethylamine-N-oxide (TMAO) is closely related to non-alcoholic fatty liver disease (NAFLD). The conversion of TMA to TMAO is mainly catalyzed by flavin-containing monooxygenases 3 (FMO3) and FMO1. In this study, we explored the role of TMA in the process of NAFLD.

Pinocembrin ameliorates acute liver failure via activating the Sirt1/PPARα pathway in vitro and in vivo.

Acute liver failure (ALF) is a life-threatening disease and affects multiple organ systems. Pro-inflammatory factors derived from macrophage plays a key role in septicemia. Pinocembrin is a natural favonoid compound, which can be extracted from honey, propolis and several other plants.

Role of SIRT1 in Hepatic Encephalopathy: In Vivo and In Vitro Studies Focusing on the NLRP3 Inflammasome.

Hepatic encephalopathy (HE) is a neuropsychiatric disorder resulting from acute or chronic liver failure. This study is aimed at investigating the therapeutic effects and mechanisms of SIRT1 in thioacetamide- (TAA-) induced rat HE models. A selective activator (CAY10602) and inhibitor (EX527) of SIRT1 were used in this study.

Trimethylamine-N-Oxide Pathway: A Potential Target for the Treatment of MAFLD.

Trimethylamine-N-oxide (TMAO) is a molecular metabolite derived from the gut flora, which has recently emerged as a candidate risk factor for metabolic dysfunction-associated fatty liver disease (MAFLD). TMAO is mainly derived from gut, where the gut microbiota converts TMA precursors into TMA, which is absorbed into the bloodstream through the intestinal mucosa, and then transformed into TMAO by hepatic flavin monooxygenases (FMOs) in the liver. High-nutrient diets rich in TMA precursors, such as red meat, eggs, and fish, are the main sources of TMAO.