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Ankita Das School of Biological Sciences, National Institute of Science Education and Research (NISER), Bhimpur-Padanpur, Jatni, Khurda, Odisha, India
Homi Bhabha National Institute, Training School Complex, Anushaktinagar, Mumbai, India

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Arka Jyoti De School of Biological Sciences, National Institute of Science Education and Research (NISER), Bhimpur-Padanpur, Jatni, Khurda, Odisha, India
Homi Bhabha National Institute, Training School Complex, Anushaktinagar, Mumbai, India

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Tanuja Mohanty School of Biological Sciences, National Institute of Science Education and Research (NISER), Bhimpur-Padanpur, Jatni, Khurda, Odisha, India
Homi Bhabha National Institute, Training School Complex, Anushaktinagar, Mumbai, India

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Palok Aich School of Biological Sciences, National Institute of Science Education and Research (NISER), Bhimpur-Padanpur, Jatni, Khurda, Odisha, India
Homi Bhabha National Institute, Training School Complex, Anushaktinagar, Mumbai, India

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hepatocytes. The second stage of this process involves cellular and molecular alterations brought on by oxidative stress and the oxidation of fatty acids in the liver, and the production of reactive oxygen species (ROS) as a result of numerous factors

Article Type:
Review Article
Collections:
Alteration of redox homeostasis and liver diseases
DOI:
https://doi.org/10.1530/REM-23-0016
Volume/Issue:
Volume 2023: Issue 1
Open access
Salvatore Sutti Department of Health Sciences and Interdisciplinary Research Centre for Autoimmune Diseases, University of East Piedmont, Novara, Italy

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Emanuele Albano Department of Health Sciences and Interdisciplinary Research Centre for Autoimmune Diseases, University of East Piedmont, Novara, Italy

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). This indicates that the presence of liver inflammation not only is the driving force for the disease evolution to cirrhosis and HCC but might also specifically contribute to extrahepatic injury. Oxidative stress in NAFLD/NASH The involvement of

Article Type:
Review Article
Collections:
Alteration of redox homeostasis and liver diseases
DOI:
https://doi.org/10.1530/REM-22-0002
Volume/Issue:
Volume 2022: Issue 1
Open access
Francesco Bellanti Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy

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Gianluigi Vendemiale Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy

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Gaetano Serviddio Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy

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liver regeneration after PHx requires NRF2, since its inactivation leads to oxidative stress-related insulin resistance, impairing the activation of anti-apoptotic and pro-mitogenic pathways ( Beyer et al. 2008 ). Of interest, NRF2 is dynamically

Article Type:
Review Article
Collections:
Alteration of redox homeostasis and liver diseases
DOI:
https://doi.org/10.1530/REM-22-0008
Volume/Issue:
Volume 2022: Issue 1
Open access
Kota Saito Department of Molecular Pathobiology, Faculty of Pharmaceutical Sciences, Kyushu University, Maidashi Higashi-ku, Fukuoka, Japan

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Yuta Matsuoka Center for Cancer Immunotherapy and Immunobiology, Graduate School of Medicine, Kyoto University, Kawahara-cho, Shogoin, Sakyo-ku, Kyoto, Japan

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Masami Abe Department of Molecular Pathobiology, Faculty of Pharmaceutical Sciences, Kyushu University, Maidashi Higashi-ku, Fukuoka, Japan

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Nao Kato Department of Molecular Pathobiology, Faculty of Pharmaceutical Sciences, Kyushu University, Maidashi Higashi-ku, Fukuoka, Japan

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Kazushi Morimoto Department of Molecular Pathobiology, Faculty of Pharmaceutical Sciences, Kyushu University, Maidashi Higashi-ku, Fukuoka, Japan

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Ken-ichi Yamada Department of Molecular Pathobiology, Faculty of Pharmaceutical Sciences, Kyushu University, Maidashi Higashi-ku, Fukuoka, Japan

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al. 2018 ). Conventionally, the ‘two-hit theory’ has been proposed as the molecular mechanism involved in NASH pathogenesis ( Day and James, 1998 ). This theory suggests that after steatosis, which is the ‘first hit’, oxidative stress promotes

Article Type:
Research Article
Collections:
Alteration of redox homeostasis and liver diseases
DOI:
https://doi.org/10.1530/REM-22-0024
Volume/Issue:
Volume 2023: Issue 1
Open access