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Antioxidants
Special Issues
Antioxidants Therapy and Oxidative Stress in Non-alcoholic Fatty Liver Disease
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Antioxidants Therapy and Oxidative Stress in Non-alcoholic Fatty Liver Disease

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 2484

Special Issue Editors

Dr. Jacek Kasznicki

E-Mail Website
Guest Editor
Department of Internal Diseases, Diabetology and Clinical Pharmacology, Medical University of Lodz, Lodz, Poland
Interests: NAFLD; oxidative stress; metabolic disorders
Dr. Melania Mikołajczyk-Solińska

E-Mail Website
Guest Editor Assistant
Department of Internal Diseases, Diabetology and Clinical Pharmacology, Medical University of Lodz, Lodz, Poland
Interests: diabetology; internal medicine; diabetes; clinical pharmacology

Special Issue Information

Dear Colleagues,

Recent meta-analyses show that the global prevalence of NAFLD is about 30%, making it the leading cause of liver-related morbidity and mortality. Despite this fact, and intensive basic and clinical research, the etiology of NAFLD is still not fully elucidated. Accumulating data gathered in recent years has provided evidence that oxidative stress is the main contributor to hepatic cell injury and death in patients with NAFLD. The modifications of the oxidant/antioxidant equilibrium affect multiple organelles. It leads to not only to peroxidation of different lipids, but also dysfunction of mitochondria and endoplasmic reticulum stress. Oxidative damage may be counteracted by the antioxidant response, which may, however, also be impaired in patients with NAFLD. Nevertheless, the translation of data gathered in preclinical studies to clinical knowledge is never easy. That is why, although we know that oxidative stress is the main contributor to the development of NAFLD, we do not have clinically approved therapies with antioxidants that target specific reactive oxygen species.

This Special Issue will cover all aspects of the role of oxidative stress and antioxidant response in the development of NAFLD and its complications. It also aims to provide knowledge of the new therapeutic targets and antioxidant interventions in NAFLD. This Special Issue invites the submission of original research, review articles, and meta-analyses.

We look forward to receiving your contributions.

Dr. Jacek Kasznicki
Guest Editor

Dr. Melania Mikołajczyk-Solińska
Guest Editor Assistant

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • NAFLD
  • oxidative stress
  • antioxidant defence
  • antioxidants
  • inflammation
  • mitochondria
  • endoplasmic reticulum
  • treatment of NAFLD
  • hepatotoxicity

Published Papers (2 papers)

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Research

22 pages, 9168 KiB  
Article
Role of Mitochondrial Reactive Oxygen Species-Mediated Chaperone-Mediated Autophagy and Lipophagy in Baicalin and N-Acetylcysteine Mitigation of Cadmium-Induced Lipid Accumulation in Liver
by Jian Sun, Yan Chen, Tao Wang, Waseem Ali, Yonggang Ma, Zongping Liu and Hui Zou
Antioxidants 2024, 13(1), 115; https://doi.org/10.3390/antiox13010115 - 17 Jan 2024
Viewed by 948
Abstract
Cadmium (Cd) is a major health concern globally and can accumulate and cause damage in the liver for which there is no approved treatment. Baicalin and N-acetylcysteine (NAC) have been found to have protective effects against a variety of liver injuries, but it [...] Read more.
Cadmium (Cd) is a major health concern globally and can accumulate and cause damage in the liver for which there is no approved treatment. Baicalin and N-acetylcysteine (NAC) have been found to have protective effects against a variety of liver injuries, but it is not clear whether their combined use is effective in preventing and treating Cd-induced lipid accumulation. The study found that Cd increased the production of mitochondrial reactive oxygen species (mROS) and elevated the level of chaperone-mediated autophagy (CMA). Interestingly, mROS-mediated CMA exacerbates the Cd-induced inhibition of lipophagy. Baicalin and NAC counteracted inhibition of lipophagy by attenuating Cd-induced CMA, suggesting an interplay between CMA elevation, mitochondrial destruction, and mROS formation. Maintaining the stability of mitochondrial structure and function is essential for alleviating Cd-induced lipid accumulation in the liver. Choline is an essential component of the mitochondrial membrane and is responsible for maintaining its structure and function. Mitochondrial transcriptional factor A (TFAM) is involved in mitochondrial DNA transcriptional activation and replication. Our study revealed that the combination of baicalin and NAC can regulate choline metabolism through TFAM and thereby maintain mitochondrial structure and functionality. In summary, the combination of baicalin and NAC plays a more beneficial role in alleviating Cd-induced lipid accumulation than the drug alone, and the combination of baicalin and NAC can stabilize mitochondrial structure and function and inhibit mROS-mediated CMA through TFAM-choline, thereby promoting lipophagy to alleviate Cd-induced lipid accumulation. Full article
(This article belongs to the Special Issue Antioxidants Therapy and Oxidative Stress in Non-alcoholic Fatty Liver Disease)
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0 pages, 5902 KiB  
Article
Extracellular Superoxide Dismutase Attenuates Hepatic Oxidative Stress in Nonalcoholic Fatty Liver Disease through the Adenosine Monophosphate-Activated Protein Kinase Activation
by Heechul Nam, Ji Hee Lim, Tae Woo Kim, Eun Nim Kim, Sae-Jong Oum, Si Hyun Bae and Cheol Whee Park
Antioxidants 2023, 12(12), 2040; https://doi.org/10.3390/antiox12122040 - 24 Nov 2023
Viewed by 1218
Abstract
Oxidative stress is key in type 2 diabetes-associated nonalcoholic fatty liver disease (NAFLD). We explored whether extracellular superoxide dismutase (EC-SOD) activates adenosine monophosphate-activated protein kinase (AMPK) to enhance antioxidant synthesis and lipid metabolism in NAFLD. Human recombinant EC-SOD (hEC-SOD) was administered to 8-week-old [...] Read more.
Oxidative stress is key in type 2 diabetes-associated nonalcoholic fatty liver disease (NAFLD). We explored whether extracellular superoxide dismutase (EC-SOD) activates adenosine monophosphate-activated protein kinase (AMPK) to enhance antioxidant synthesis and lipid metabolism in NAFLD. Human recombinant EC-SOD (hEC-SOD) was administered to 8-week-old male C57BLKS/J db/db mice through intraperitoneal injection once a week for 8 weeks. Target molecules involved in oxidative stress and lipid metabolism were investigated. hEC-SOD improved insulin resistance and systemic and hepatic oxidative stress characterized by increases in urinary 8-hydroxy-deoxyguanosine and 8-isoprostane levels in db/db mice and a decrease in DHE expression in the liver, respectively. Hepatic SOD3 expression in db/db mice was reversed by hEC-SOD, which improved hepatic steatosis, inflammation with M2 polarization, apoptosis, autophagy, fibrosis and lipid metabolism in db/db mice, as reflected by the changes in serum and hepatic markers, monocyte chemoattractant protein-1, tumor necrosis factor-α, TUNEL-positive cells, Bcl-2/BAX ratio, beclin1 and LC3-II/LC3-1. At the molecular level, hEC-SOD increased phosphorylated-AMPK related to CaMKKß, activation of peroxisome proliferative-activated receptor-gamma coactivator (PGC)-1α and dephosphorylation of forkhead box O (FoxO)1 and their subsequent downstream signaling. In HepG2Cs cells using AMPKα1 and AMPKα2 siRNA, hEC-SOD demonstrated a protective effect via the direct activation of both AMPK-PGC-1α and AMPK-FoxO1. EC-SOD might be a potential therapeutic agent for NAFLD through the activation of AMPK-PGC-1α and AMPK-FoxO1 signaling in hepatocytes, which modulates lipid metabolism, leading to anti-inflammatory, antioxidative and antiapoptotic effects and improving autophagy in the liver. Full article
(This article belongs to the Special Issue Antioxidants Therapy and Oxidative Stress in Non-alcoholic Fatty Liver Disease)
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