Kuo Du
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View article: Author Correction: Targeting senescent hepatocytes for treatment of metabolic dysfunction-associated steatotic liver disease and multi-organ dysfunction
Author Correction: Targeting senescent hepatocytes for treatment of metabolic dysfunction-associated steatotic liver disease and multi-organ dysfunction Open
View article: Targeting senescent hepatocytes for treatment of metabolic dysfunction-associated steatotic liver disease and multi-organ dysfunction
Targeting senescent hepatocytes for treatment of metabolic dysfunction-associated steatotic liver disease and multi-organ dysfunction Open
View article: A systemic effect for liver senescence
A systemic effect for liver senescence Open
View article: The senescence-associated secretome of Hedgehog-deficient hepatocytes drives MASLD progression
The senescence-associated secretome of Hedgehog-deficient hepatocytes drives MASLD progression Open
The burden of senescent hepatocytes correlates with the severity of metabolic dysfunction-associated steatotic liver disease (MASLD), but the mechanisms driving senescence and how it exacerbates MASLD are poorly understood. Hepatocytes exp…
View article: Plasticity, heterogeneity, and multifunctionality of hepatic stellate cells in liver pathophysiology
Plasticity, heterogeneity, and multifunctionality of hepatic stellate cells in liver pathophysiology Open
HSCs, the resident pericytes of the liver, have consistently been at the forefront of liver research due to their crucial roles in various hepatic pathological processes. Prior literature often depicted HSCs in a binary framework, categori…
View article: Antagonizing the irreversible thrombomodulin-initiated proteolytic signaling alleviates age-related liver fibrosis via senescent cell killing
Antagonizing the irreversible thrombomodulin-initiated proteolytic signaling alleviates age-related liver fibrosis via senescent cell killing Open
View article: Targeting senescent hepatocytes using the thrombomodulin-PAR1 inhibitor vorapaxar ameliorates NAFLD progression
Targeting senescent hepatocytes using the thrombomodulin-PAR1 inhibitor vorapaxar ameliorates NAFLD progression Open
Background and Aims: Senescent hepatocytes accumulate in parallel with fibrosis progression during NASH. The mechanisms that enable progressive expansion of nonreplicating cell populations and the significance of that process in determinin…
View article: Targeting YAP-mediated HSC death susceptibility and senescence for treatment of liver fibrosis
Targeting YAP-mediated HSC death susceptibility and senescence for treatment of liver fibrosis Open
Background and Aims: Liver fibrosis results from the accumulation of myofibroblasts (MFs) derived from quiescent HSCs, and yes-associated protein (YAP) controls this state transition. Although fibrosis is also influenced by HSC death and s…
View article: Hepatocyte Smoothened Activity Controls Susceptibility to Insulin Resistance and Nonalcoholic Fatty Liver Disease
Hepatocyte Smoothened Activity Controls Susceptibility to Insulin Resistance and Nonalcoholic Fatty Liver Disease Open
View article: Inhibiting xCT/SLC7A11 induces ferroptosis of myofibroblastic hepatic stellate cells but exacerbates chronic liver injury
Inhibiting xCT/SLC7A11 induces ferroptosis of myofibroblastic hepatic stellate cells but exacerbates chronic liver injury Open
Background & Aims The outcome of liver injury is dictated by factors that control the accumulation of myofibroblastic (activated) hepatic stellate cells (MF‐HSCs) but therapies that specifically block this process have not been discovered.…
View article: Mitochondrial protein adduct and superoxide generation are prerequisites for early activation of c-jun N-terminal kinase within the cytosol after an acetaminophen overdose in mice
Mitochondrial protein adduct and superoxide generation are prerequisites for early activation of c-jun N-terminal kinase within the cytosol after an acetaminophen overdose in mice Open
View article: Issue Cover
Issue Cover Open
The cover image is based on the Original Article Succinate-GPR-91 Receptor Signaling Is Responsible for Nonalcoholic Steatohepatitis-Associated Fibrosis: Effects of DHA Supplementation by Jian Wu, Ying Wang, Li Xie et al., https://doi.org/…
View article: Epithelial splicing regulatory protein 2–mediated alternative splicing reprograms hepatocytes in severe alcoholic hepatitis
Epithelial splicing regulatory protein 2–mediated alternative splicing reprograms hepatocytes in severe alcoholic hepatitis Open
Severe alcoholic hepatitis (SAH) is a deadly liver disease without an effective medical therapy. Although SAH mortality is known to correlate with hepatic accumulation of immature liver cells, why this occurs and how it causes death are un…
View article: Succinate‐GPR‐91 receptor signalling is responsible for nonalcoholic steatohepatitis‐associated fibrosis: Effects of DHA supplementation
Succinate‐GPR‐91 receptor signalling is responsible for nonalcoholic steatohepatitis‐associated fibrosis: Effects of DHA supplementation Open
Background and aims Treatment of non‐alcoholic steatohepatitis (NASH) is challenging, because suppressing fibrotic progression has not been achieved consistently by drug candidates currently in clinical trials. The aim of this study was to…
View article: Increased Glutaminolysis Marks Active Scarring in Nonalcoholic Steatohepatitis Progression
Increased Glutaminolysis Marks Active Scarring in Nonalcoholic Steatohepatitis Progression Open
View article: Inhibiting xCT/SLC7A11 induces ferroptosis of myofibroblastic hepatic stellate cells and protects against liver fibrosis
Inhibiting xCT/SLC7A11 induces ferroptosis of myofibroblastic hepatic stellate cells and protects against liver fibrosis Open
Background and Aims Liver fibrosis develops in the context of excessive oxidative stress, cell death and accumulation of myofibroblasts (MFs) derived from hepatic stellate cells (HSCs). Ferroptosis is a type of regulated cell death that ca…
View article: Single-Cell RNA Sequencing Identifies Yes-Associated Protein 1–Dependent Hepatic Mesothelial Progenitors in Fibrolamellar Carcinoma
Single-Cell RNA Sequencing Identifies Yes-Associated Protein 1–Dependent Hepatic Mesothelial Progenitors in Fibrolamellar Carcinoma Open
View article: Tu1566 – Dysregulated Dna Methylation of Fgfr2, Casp1, and Bcat1 Associates with Nonalcoholic Fatty Liver Disease Severity and Can Be Identified in Peripheral Blood
Tu1566 – Dysregulated Dna Methylation of Fgfr2, Casp1, and Bcat1 Associates with Nonalcoholic Fatty Liver Disease Severity and Can Be Identified in Peripheral Blood Open
View article: Hedgehog-YAP Signaling Pathway Regulates Glutaminolysis to Control Activation of Hepatic Stellate Cells
Hedgehog-YAP Signaling Pathway Regulates Glutaminolysis to Control Activation of Hepatic Stellate Cells Open
View article: MITOCHONDRIAL OXIDATIVE STRESS AND BIOGENESIS DURING ACETAMINOPHEN HEPATOTOXICITY
MITOCHONDRIAL OXIDATIVE STRESS AND BIOGENESIS DURING ACETAMINOPHEN HEPATOTOXICITY Open
Acetaminophen (APAP) overdose causes severe hepatotoxicity in animals and humans. Although numerous studies have established the existence of an extensive oxidative stress during APAP hepatotoxicity, its source, pathophysiological roles an…
View article: Differential susceptibility to acetaminophen-induced liver injury in sub-strains of C57BL/6 mice: 6N versus 6J
Differential susceptibility to acetaminophen-induced liver injury in sub-strains of C57BL/6 mice: 6N versus 6J Open
View article: Dual Role of Epidermal Growth Factor Receptor in Liver Injury and Regeneration after Acetaminophen Overdose in Mice
Dual Role of Epidermal Growth Factor Receptor in Liver Injury and Regeneration after Acetaminophen Overdose in Mice Open
Epidermal growth factor receptor (EGFR) plays a crucial role in hepatocyte proliferation. Its role in acetaminophen (APAP)-mediated hepatotoxicity and subsequent liver regeneration is completely unknown. Role of EGFR after APAP-overdose in…
View article: Oxidative stress during acetaminophen hepatotoxicity: Sources, pathophysiological role and therapeutic potential
Oxidative stress during acetaminophen hepatotoxicity: Sources, pathophysiological role and therapeutic potential Open
View article: Editor’s Highlight: Metformin Protects Against Acetaminophen Hepatotoxicity by Attenuation of Mitochondrial Oxidant Stress and Dysfunction
Editor’s Highlight: Metformin Protects Against Acetaminophen Hepatotoxicity by Attenuation of Mitochondrial Oxidant Stress and Dysfunction Open
Overdose of acetaminophen (APAP) causes severe liver injury and even acute liver failure in both mice and human. A recent study by Kim et al. (2015, Metformin ameliorates acetaminophen hepatotoxicity via Gadd45β-dependent regulation of JNK…
View article: Removal of acetaminophen protein adducts by autophagy protects against acetaminophen-induced liver injury in mice
Removal of acetaminophen protein adducts by autophagy protects against acetaminophen-induced liver injury in mice Open
View article: Liuweiwuling tablets protect against acetaminophen hepatotoxicity: What is the protective mechanism?
Liuweiwuling tablets protect against acetaminophen hepatotoxicity: What is the protective mechanism? Open
Study of the effects of natural products, including traditional Chinese Medicines, on acetaminophen hepatotoxicity has gained considerable popularity in recent years, and some of them showed positive results and even promising therapeutic …
View article: Benzyl alcohol protects against acetaminophen hepatotoxicity by inhibiting cytochrome P450 enzymes but causes mitochondrial dysfunction and cell death at higher doses
Benzyl alcohol protects against acetaminophen hepatotoxicity by inhibiting cytochrome P450 enzymes but causes mitochondrial dysfunction and cell death at higher doses Open
View article: Mitochondrial protein adducts formation and mitochondrial dysfunction during N-acetyl-m-aminophenol (AMAP)-induced hepatotoxicity in primary human hepatocytes
Mitochondrial protein adducts formation and mitochondrial dysfunction during N-acetyl-m-aminophenol (AMAP)-induced hepatotoxicity in primary human hepatocytes Open
View article: Pathophysiological significance of c-jun<i>N</i>-terminal kinase in acetaminophen hepatotoxicity
Pathophysiological significance of c-jun<i>N</i>-terminal kinase in acetaminophen hepatotoxicity Open
JNK is a potential therapeutic target for APAP poisoning. However, controversies still exist regarding its actual role in APAP hepatotoxicity. Future studies are warranted for more in-depth testing of specific inhibitors in well-defined pr…
View article: Benzyl Alcohol: A novel treatment for acetaminophen overdose?
Benzyl Alcohol: A novel treatment for acetaminophen overdose? Open
Potential conflict of interest: Nothing to report. To the Editor: We read with interest the recent article by Cai et al. suggesting that "benzyl alcohol (BA) may prove to be a useful adjunct in the treatment of APAP and other forms of ster…