Superoxide anion radicals activate hepatic stellate cells after entry through chloride channels: A new target in liver fibrosis

Hartog, G.J.M. den; Qi, Shusen; Tilburg, Jonathan H.O. van; Koek, Ger H.; Bast, Aalt

doi:10.1016/j.ejphar.2013.12.033

Cited by 24 publications

(18 citation statements)

References 23 publications

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“…Antioxidant therapeutics that particularly target mitochondrial damage (Kang et al, ), LPO and its products (Tahan et al, ), and HSC activation (den Hartog et al, ) have been reported to reduce fibrosis in experimental models. Melatonin administration is an effective therapeutic choice in targeting liver fibrosis (Mortezaee, Khanlarkhani, et al, ).…”

Section: The Role Of Oxidative Stress In Liver Fibrosis and Cirrhosismentioning

confidence: 99%

“…Mechanism of oxidative stress‐induced liver fibrogenesis and the protection by melatonin against carbon tetrachloride (CCl 4 ). Reactive oxygen species (ROS) play a key role in the pathogenesis of liver fibrosis (den Hartog et al, ). A likely candidate for the sole or main profibrotic species is superoxide (

{normalO}_{2}^{\cdot -}

) (den Hartog et al, ).…”

Section: The Role Of Oxidative Stress In Liver Fibrosis and Cirrhosismentioning

confidence: 99%

“…Reactive oxygen species (ROS) play a key role in the pathogenesis of liver fibrosis (den Hartog et al, ). A likely candidate for the sole or main profibrotic species is superoxide (

{normalO}_{2}^{\cdot -}

) (den Hartog et al, ). ROS stimulate Kupffer cells (KCs) to produce profibrogenic mediators (Sánchez‐Valle et al, ), such as transforming growth factor (TGF)‐β1 and platelet‐derived growth factor (PDGF) that further activate hepatic stellate cells (HSCs) (Rivera et al, ) through transformation of HSCs into myofibroblasts (Yang, Chang, Hong, Hung, & Chuang, ).…”

Section: The Role Of Oxidative Stress In Liver Fibrosis and Cirrhosismentioning

confidence: 99%

“…ROS stimulate Kupffer cells (KCs) to produce profibrogenic mediators (Sánchez‐Valle et al, ), such as transforming growth factor (TGF)‐β1 and platelet‐derived growth factor (PDGF) that further activate hepatic stellate cells (HSCs) (Rivera et al, ) through transformation of HSCs into myofibroblasts (Yang, Chang, Hong, Hung, & Chuang, ).

{normalO}_{2}^{\cdot -}

also induces release of collagen and TGF‐β1 from HSCs (den Hartog et al, ).

{normalO}_{2}^{\cdot -}

is generated from enzymatic activity of xanthine oxidase (XO) (Ohta et al, ).…”

Section: The Role Of Oxidative Stress In Liver Fibrosis and Cirrhosismentioning

confidence: 99%

“…NOX2 mediates robust production of

{normalO}_{2}^{\cdot -}

in KCs (Paik et al, ).

{normalO}_{2}^{\cdot -}

enters HSCs through chloride (Cl − ) channels (den Hartog et al, ). NOX‐derived ROS induce HSC survival and associate with the propagation of activated HSCs (Jiang et al, ).…”

Section: The Role Of Oxidative Stress In Liver Fibrosis and Cirrhosismentioning

confidence: 99%

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Melatonin application in targeting oxidative‐induced liver injuries: A review

Mortezaee

Khanlarkhani

2017

Journal Cellular Physiology

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It is believed that oxidative stress is a key causing factor of liver damage induced by a variety of agents, and it is a major contributing factor in almost all conditions compromising liver function, including ischemia-reperfusion injury (IRI), nonalcoholic fatty liver disease (NAFLD), nonalcoholic steatohepatitis (NASH), liver fibrosis, liver cirrhosis, and hepatocellular carcinoma (HCC). Liver is the organ that high concentration of melatonin (N-acetyl-5-methoxytryptamine) accumulates, and it is the sole organ where circulating melatonin is metabolized. Melatonin is one of the best antioxidants that protects liver, and its metabolites also have antioxidative function. Melatonin exerts its antioxidative function directly through its radical scavenging ability and indirectly through stimulation of antioxidant enzymes. The antioxidative response from melatonin in liver affects from various factors, including its dosage, route, time and duration of administration, the type of oxidative-induced agent and species aging. This indoleamine is also an effective and promising antioxidative choice for targeting liver IRI, NAFLD, NASH, fibrosis, cirrhosis, and HCC.

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Section: The Role Of Oxidative Stress In Liver Fibrosis and Cirrhosismentioning

confidence: 99%

{normalO}_{2}^{\cdot -}

) (den Hartog et al, ).…”

Section: The Role Of Oxidative Stress In Liver Fibrosis and Cirrhosismentioning

confidence: 99%

“…Reactive oxygen species (ROS) play a key role in the pathogenesis of liver fibrosis (den Hartog et al, ). A likely candidate for the sole or main profibrotic species is superoxide (

{normalO}_{2}^{\cdot -}

Section: The Role Of Oxidative Stress In Liver Fibrosis and Cirrhosismentioning

confidence: 99%

{normalO}_{2}^{\cdot -}

also induces release of collagen and TGF‐β1 from HSCs (den Hartog et al, ).

{normalO}_{2}^{\cdot -}

is generated from enzymatic activity of xanthine oxidase (XO) (Ohta et al, ).…”

Section: The Role Of Oxidative Stress In Liver Fibrosis and Cirrhosismentioning

confidence: 99%

“…NOX2 mediates robust production of

{normalO}_{2}^{\cdot -}

in KCs (Paik et al, ).

{normalO}_{2}^{\cdot -}

enters HSCs through chloride (Cl − ) channels (den Hartog et al, ). NOX‐derived ROS induce HSC survival and associate with the propagation of activated HSCs (Jiang et al, ).…”

Section: The Role Of Oxidative Stress In Liver Fibrosis and Cirrhosismentioning

confidence: 99%

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Melatonin application in targeting oxidative‐induced liver injuries: A review

Mortezaee

Khanlarkhani

2017

Journal Cellular Physiology

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Hepatocyte TMEM16A Deletion Retards NAFLD Progression by Ameliorating Hepatic Glucose Metabolic Disorder

et al. 2020

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Nonalcoholic fatty liver disease (NAFLD) is the most prevalent form of chronic liver disease, and the mechanisms underpinning its pathogenesis have not been completely established. Transmembrane member 16A (TMEM16A), a component of the Ca2+‐activated chloride channel (CaCC), has recently been implicated in metabolic events. Herein, TMEM16A is shown to be responsible for CaCC activation in hepatocytes and is increased in liver tissues of mice and patients with NAFLD. Hepatocyte‐specific ablation of TMEM16A in mice ameliorates high‐fat diet‐induced obesity, hepatic glucose metabolic disorder, steatosis, insulin resistance, and inflammation. In contrast, hepatocyte‐specific TMEM16A transgenic mice exhibit the opposite phenotype. Mechanistically, hepatocyte TMEM16A interacts with vesicle‐associated membrane protein 3 (VAMP3) to induce its degradation, suppressing the formation of the VAMP3/syntaxin 4 and VAMP3/synaptosome‐associated protein 23 complexes. This leads to the impairment of hepatic glucose transporter 2 (GLUT2) translocation and glucose uptake. Notably, VAMP3 overexpression restrains the functions of hepatocyte TMEM16A in blocking GLUT2 translocation and promoting lipid deposition, insulin resistance, and inflammation. In contrast, VAMP3 knockdown reverses the beneficial effects of TMEM16A downregulation. This study demonstrates a role for TMEM16A in NAFLD and suggests that inhibition of hepatic TMEM16A or disruption of TMEM16A/VAMP3 interaction may provide a new potential therapeutic strategy for NAFLD.

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RETRACTED: Post‐treatment of melatonin with CCl₄ better reduces fibrogenic and oxidative changes in liver than melatonin co‐treatment

Mortezaee

Majidpoor

Daneshi

et al. 2017

J of Cellular Biochemistry

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Therapeutic effects of melatonin (MEL) in targeting CCl -induced liver fibrosis has been widely known, but there is no study comparing oxidative and fibrogenic changes in co- and post-treatment of MEL with CCl , which was further aimed in this experiment. Male SD rats were injected with CCl (1 mL/kg/i.p./daily) dissolved 1:1 in olive oil for 1 month. Some animals received MEL (20 mg/kg/i.p./daily) diluted in 1 mL PBS in combination with CCl (co-treatment), and some rats were treated with MEL, beginning with injection of the last dose of CCl for one month (post-treatment). The groups were control, CCl , CCl -co vehicle, CCl -post vehicle, post-CCl , MEL co-treatment, and MEL post-treatment. MEL post-treatment group showed significantly lower lipid deposition, serum malondialdehyde (MDA), serum alanine aminotransferase (ALT), and liver hydroxyproline. This group also had low expressions of Bax and transforming growth factor-β1 (TGF-β1). MEL post-treatment group revealed higher sera levels of albumin, superoxide dismutase (SOD) and glutathione peroxidase (GPx). Expression levels of metalloproteinase-13 (MMP-13) and Bcl2 was also higher in this group (P ≤ 0.05 vs co-treatment). Results of the present study indicated that MEL post-treatment is more powerful in reduction of CCl -induced liver fibrosis through reduction of oxidative stress and maintenance of matrix balance.

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Superoxide anion radicals activate hepatic stellate cells after entry through chloride channels: A new target in liver fibrosis

Cited by 24 publications

References 23 publications

Melatonin application in targeting oxidative‐induced liver injuries: A review

Melatonin application in targeting oxidative‐induced liver injuries: A review

Hepatocyte TMEM16A Deletion Retards NAFLD Progression by Ameliorating Hepatic Glucose Metabolic Disorder

RETRACTED: Post‐treatment of melatonin with CCl₄ better reduces fibrogenic and oxidative changes in liver than melatonin co‐treatment

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Superoxide anion radicals activate hepatic stellate cells after entry through chloride channels: A new target in liver fibrosis

Cited by 24 publications

References 23 publications

Melatonin application in targeting oxidative‐induced liver injuries: A review

Melatonin application in targeting oxidative‐induced liver injuries: A review

Hepatocyte TMEM16A Deletion Retards NAFLD Progression by Ameliorating Hepatic Glucose Metabolic Disorder

RETRACTED: Post‐treatment of melatonin with CCl4 better reduces fibrogenic and oxidative changes in liver than melatonin co‐treatment

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RETRACTED: Post‐treatment of melatonin with CCl₄ better reduces fibrogenic and oxidative changes in liver than melatonin co‐treatment