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pubmed, article, google, scholar, cas, liver, ferroptosis, injury, central, mitochondrial, cell, acetaminophen, mitochondria, druginduced, vdac, hepatotoxicity, apapinduced, disease, httpsdoiorgs, toxicol, shanghai, acetaminopheninduced, acute, iron, biol, research, mao, chen, analysis, data, dysfunction, acid, fatty, hepatocytes, hepatology, chem, jaeschke, clinical, wang, university, function, content, oligomerization, niu, mice, cardiolipin, access, death, china, privacy,

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voltage-dependent anion channel month download article/chapter acetaminophen-induced hepatic necrosis apap-induced liver injury acetaminophen-induced liver injury fatty acid beta-oxidation drug-induced hepatic injuries acute liver injury drug-induced liver injury acetaminophen-induced liver toxicity drive apap-induced ferroptosis acute acetaminophen toxicity apap-induced mitochondrial dysfunction high-level local universities energy-dependent accumulation ccl4-induced lipid peroxidation long-chain hydroxydicarboxylic aciduria kullak-ublick ga biochim biophys acta article cell biology redox-dependent gating apap-induced ferroptosis acetaminophen-induced hepatotoxicity full article pdf french population-based study cell death dis drug-induced hepatotoxicity autoimmune liver disease cell mol neurobiol hepatic transcriptome profiling liver biopsy samples related subjects human liver samples explore underlying mechanisms glutamate-induced oxytosis mito-tempo protects privacy choices/manage cookies oligomerization inhibitor vbit-12 check access instant access european economic area apap overdose led apap-injured mice clinical research center lipids health dis liver injury expert rev hematol bjornsson es mengchao hepatobiliary hospital innovative research team

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• Ferroptosis and acetaminophen hepatotoxicity - are we going down another rabbit hole?

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         headline:Protecting mitochondria via inhibiting VDAC1 oligomerization alleviates ferroptosis in acetaminophen-induced acute liver injury
         description:Acetaminophen (APAP) overdose is a common cause of drug-induced liver injury (DILI). Ferroptosis has been recently implicated in APAP-induced liver injury (AILI). However, the functional role and underlying mechanisms of mitochondria in APAP-induced ferroptosis are unclear. In this study, the voltage-dependent anion channel (VDAC) oligomerization inhibitor VBIT-12 and ferroptosis inhibitors were injected via tail vein in APAP-injured mice. Targeted metabolomics and untargeted lipidomic analyses were utilized to explore underlying mechanisms of APAP-induced mitochondrial dysfunction and subsequent ferroptosis. As a result, APAP overdose led to characteristic changes generally observed in ferroptosis. The use of ferroptosis inhibitor ferrostatin-1 (or UAMC3203) and iron chelator deferoxamine further confirmed that ferroptosis was responsible for AILI. Mitochondrial dysfunction, which is associated with the tricarboxylic acid cycle and fatty acid β-oxidation suppression, may drive APAP-induced ferroptosis in hepatocytes. APAP overdose induced VDAC1 oligomerization in hepatocytes, and protecting mitochondria via VBIT-12 alleviated APAP-induced ferroptosis. Ceramide and cardiolipin levels were increased via UAMC3203 or VBIT-12 in APAP-induced ferroptosis in hepatocytes. Knockdown of Smpd1 and Taz expression responsible for ceramide and cardiolipin synthesis, respectively, aggravated APAP-induced mitochondrial dysfunction and ferroptosis in hepatocytes, whereas Taz overexpression protected against these processes. By immunohistochemical staining, we found that levels of 4-hydroxynonenal (4-HNE) protein adducts were increased in the liver biopsy samples of patients with DILI compared to that in those of patients with autoimmune liver disease, chronic viral hepatitis B, and non-alcoholic fatty liver disease (NAFLD). In summary, protecting mitochondria via inhibiting VDAC1 oligomerization attenuated hepatocyte ferroptosis by restoring ceramide and cardiolipin content in AILI.
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      description:Acetaminophen (APAP) overdose is a common cause of drug-induced liver injury (DILI). Ferroptosis has been recently implicated in APAP-induced liver injury (AILI). However, the functional role and underlying mechanisms of mitochondria in APAP-induced ferroptosis are unclear. In this study, the voltage-dependent anion channel (VDAC) oligomerization inhibitor VBIT-12 and ferroptosis inhibitors were injected via tail vein in APAP-injured mice. Targeted metabolomics and untargeted lipidomic analyses were utilized to explore underlying mechanisms of APAP-induced mitochondrial dysfunction and subsequent ferroptosis. As a result, APAP overdose led to characteristic changes generally observed in ferroptosis. The use of ferroptosis inhibitor ferrostatin-1 (or UAMC3203) and iron chelator deferoxamine further confirmed that ferroptosis was responsible for AILI. Mitochondrial dysfunction, which is associated with the tricarboxylic acid cycle and fatty acid β-oxidation suppression, may drive APAP-induced ferroptosis in hepatocytes. APAP overdose induced VDAC1 oligomerization in hepatocytes, and protecting mitochondria via VBIT-12 alleviated APAP-induced ferroptosis. Ceramide and cardiolipin levels were increased via UAMC3203 or VBIT-12 in APAP-induced ferroptosis in hepatocytes. Knockdown of Smpd1 and Taz expression responsible for ceramide and cardiolipin synthesis, respectively, aggravated APAP-induced mitochondrial dysfunction and ferroptosis in hepatocytes, whereas Taz overexpression protected against these processes. By immunohistochemical staining, we found that levels of 4-hydroxynonenal (4-HNE) protein adducts were increased in the liver biopsy samples of patients with DILI compared to that in those of patients with autoimmune liver disease, chronic viral hepatitis B, and non-alcoholic fatty liver disease (NAFLD). In summary, protecting mitochondria via inhibiting VDAC1 oligomerization attenuated hepatocyte ferroptosis by restoring ceramide and cardiolipin content in AILI.
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            address:
               name:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China
               type:PostalAddress
            type:Organization
      name:Jing Li
      affiliation:
            name:Shanghai Jiao Tong University
            address:
               name:Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Renji Hospital, School of Medicine, Shanghai Institute of Digestive Disease, Shanghai Jiao Tong University, Shanghai, China
               type:PostalAddress
            type:Organization
      name:Yufan Zheng
      affiliation:
            name:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University
            address:
               name:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China
               type:PostalAddress
            type:Organization
      name:Ning Sun
      affiliation:
            name:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University
            address:
               name:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China
               type:PostalAddress
            type:Organization
      name:Xin Zhang
      affiliation:
            name:Fudan University Zhongshan Hospital
            address:
               name:Department of Pathology, Fudan University Zhongshan Hospital, Shanghai, China
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Yimin Mao
      affiliation:
            name:Shanghai Jiao Tong University
            address:
               name:Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Renji Hospital, School of Medicine, Shanghai Institute of Digestive Disease, Shanghai Jiao Tong University, Shanghai, China
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Xiaobo Li
      url:http://orcid.org/0000-0001-7737-1721
      affiliation:
            name:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University
            address:
               name:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China
      name:Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Renji Hospital, School of Medicine, Shanghai Institute of Digestive Disease, Shanghai Jiao Tong University, Shanghai, China
      name:Department of Hepatology, Mengchao Hepatobiliary Hospital of Fujian Medical University, Fuzhou, China
      name:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China
      name:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China
      name:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China
      name:Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Renji Hospital, School of Medicine, Shanghai Institute of Digestive Disease, Shanghai Jiao Tong University, Shanghai, China
      name:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China
      name:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China
      name:Department of Pathology, Fudan University Zhongshan Hospital, Shanghai, China
      name:Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Renji Hospital, School of Medicine, Shanghai Institute of Digestive Disease, Shanghai Jiao Tong University, Shanghai, China
      name:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China
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