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Antioxidants
Special Issues
Lipid Metabolism and Redox Regulation in Diseases
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Lipid Metabolism and Redox Regulation in Diseases

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: closed (31 January 2023) | Viewed by 7666

Special Issue Editor

Prof. Dr. Jihong Han

E-Mail Website
Guest Editor
Key Laboratory of Metabolism and Regulation for Major Diseases of Anhui Higher Education Institutes, College of Food and Biological Engineering, Hefei University of Technology, Hefei 230601, China
Interests: glucose and lipid metabolism in diseases; especially cardiovascular diseases; diabetes; nonalcoholic fatty liver disease; obesity

Special Issue Information

Dear Colleagues,

Redox balance is one the bases of intracellular homeostasis. Redox reactions are related to the generation and scavenging mechanisms of reactive oxygen species (ROS), and determine the intracellular redox status. In recent years, a great deal of evidence has emerged showing that ROS play a key role in regulating cellular lipid metabolism, and participate in the occurrence and development of lipid-metabolism-related diseases. In many pathological processes, such as such as obesity, nonalcoholic fatty liver, neurodegeneration and cardiovascular dysfunction, the interaction between redox homeostasis and cellular metabolism/functions is impaired.

Therefore, understanding the lipid metabolism and redox regulation in diseases, particularly in cardiovascular disease (e.g., atherosclerosis and heart injury) is very helpful to the development of new and promising therapies. The purpose of this Special Issue titled "Lipid Metabolism and Redox Regulation in Diseases" is to collect original research articles and recent reviews on basic and applied research, focusing on the crosstalk between lipid metabolism and redox regulation during disease processes. Studies may focus on but not be limited to the following aspects: The role of lipid metabolism and redox regulation in the formation of macrophage/foam cells and lesions; endothelial injury and the interaction between endothelial cells and monocytes/macrophages; the impact of synthetic reagents and natural production on lipid metabolism and redox regulation; the identification of new signaling pathways in lipid metabolism and redox regulation; and more. We welcome the submission of studies related to the aspects listed above in this advanced field.

Prof. Dr. Jihong Han
Guest Editor

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

  • lipid oxidation and metabolism
  • oxidative stress and inflammation
  • molecular mechanisms
  • antioxidant and application
  • mitochondrial oxidative stress
  • ROS species
  • redox regulation
  • cell metabolism
  • cellular signaling

Published Papers (3 papers)

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Research

12 pages, 1759 KiB  
Article
Carbon Nanodots Attenuate Lipid Peroxidation in the LDL Receptor Knockout Mouse Brain
by Keith M. Erikson, Kristina El-Khouri, Radmila Petric, Chenhao Tang, Jinlan Chen, Delicia Esther Cardenas Vasquez, Steve C. Fordahl and Zhenquan Jia
Antioxidants 2023, 12(5), 1081; https://doi.org/10.3390/antiox12051081 - 11 May 2023
Viewed by 1672
Abstract
Abnormal cholesterol metabolism can lead to oxidative stress in the brain. Low-density lipoprotein receptor (LDLr) knockout mice are models for studying altered cholesterol metabolism and oxidative stress onset in the brain. Carbon nanodots are a new class of carbon nanomaterials that possess antioxidant [...] Read more.
Abnormal cholesterol metabolism can lead to oxidative stress in the brain. Low-density lipoprotein receptor (LDLr) knockout mice are models for studying altered cholesterol metabolism and oxidative stress onset in the brain. Carbon nanodots are a new class of carbon nanomaterials that possess antioxidant properties. The goal of our study was to evaluate the effectiveness of carbon nanodots in preventing brain lipid peroxidation. LDLr knockout mice and wild-type C57BL/6J mice were treated with saline or 2.5 mg/kg bw of carbon nanodots for a 16-week period. Brains were removed and dissected into the cortex, midbrain, and striatum. We measured lipid peroxidation in the mouse brain tissues using the Thiobarbituric Acid Reactive Substances Assay and iron and copper concentrations using Graphite Furnace Atomic Absorption Spectroscopy. We focused on iron and copper due to their association with oxidative stress. Iron concentrations were significantly elevated in the midbrain and striatum of the LDLr knockout mice compared to the C57BL/6J mice, whereas lipid peroxidation was greatest in the midbrain and cortex of the LDLr knockout mice. Treatment with carbon nanodots in the LDLr knockout mice attenuated both the rise in iron and lipid peroxidation, but they had no negative effect in the C57BL/6J mice, indicating the anti-oxidative stress properties of carbon nanodots. We also assessed locomotor and anxiety-like behaviors as functional indicators of lipid peroxidation and found that treatment with carbon nanodots prevented the anxiety-like behaviors displayed by the LDLr knockout mice. Overall, our results show that carbon nanodots are safe and may be an effective nanomaterial for combating the harmful effects caused by lipid peroxidation. Full article
(This article belongs to the Special Issue Lipid Metabolism and Redox Regulation in Diseases)
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14 pages, 3711 KiB  
Article
Identification of AP-1 as a Critical Regulator of Glutathione Peroxidase 4 (GPX4) Transcriptional Suppression and Acinar Cell Ferroptosis in Acute Pancreatitis
by Xiaojie Ma, Xiaowu Dong, Yao Xu, Nan Ma, Mei Wei, Xiaochun Xie, Yingying Lu, Wangsen Cao, Guotao Lu and Weiqin Li
Antioxidants 2023, 12(1), 100; https://doi.org/10.3390/antiox12010100 - 31 Dec 2022
Cited by 7 | Viewed by 2573
Abstract
Glutathione peroxidase 4 (GPX4)-dependent ferroptosis in pancreatic acinar cells plays a critical role in acute pancreatitis (AP). However, potential upstream regulators of GPX4 are not well defined. Here, we observed a marked reduction in acinar GPX4 expression and ferroptotic cell death in mice [...] Read more.
Glutathione peroxidase 4 (GPX4)-dependent ferroptosis in pancreatic acinar cells plays a critical role in acute pancreatitis (AP). However, potential upstream regulators of GPX4 are not well defined. Here, we observed a marked reduction in acinar GPX4 expression and ferroptotic cell death in mice with cerulein-induced AP. To determine the critical factors involved in acinar cell ferroptosis, pancreas transcriptome data from an AP mouse model were analyzed and overlapped with predicted transcription factors of Gpx4, and an upregulated transcription factor active protein 1 (AP-1) protein, Jun, was identified. The administration of a specific ferroptosis inhibitor liproxstatin-1 alleviated AP pathology and significantly decreased Jun levels. Bioinformatic analysis indicated that the Gpx4 promoter contains a putative AP-1 binding site. Jun binds directly to the Gpx4 promoter and inhibits Gpx4 transcription under pancreatic conditions. AP-1 inhibition by a selective inhibitor SR11302 reversed GPX4 reduction and ameliorated AP pathology in a GPX4-dependent manner. Collectively, our study demonstrates that the downregulation of GPX4 by AP-1 is critical in the aggravation of acinar cell ferroptosis during the progression of AP. Strategies targeting the AP-1/GPX4 axis may be potentially effective for the prevention and treatment of AP. Full article
(This article belongs to the Special Issue Lipid Metabolism and Redox Regulation in Diseases)
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21 pages, 3195 KiB  
Article
ApoE3 vs. ApoE4 Astrocytes: A Detailed Analysis Provides New Insights into Differences in Cholesterol Homeostasis
by Erica Staurenghi, Valerio Leoni, Marco Lo Iacono, Barbara Sottero, Gabriella Testa, Serena Giannelli, Gabriella Leonarduzzi and Paola Gamba
Antioxidants 2022, 11(11), 2168; https://doi.org/10.3390/antiox11112168 - 1 Nov 2022
Cited by 5 | Viewed by 2975
Abstract
The strongest genetic risk factor for sporadic Alzheimer’s disease (AD) is the presence of the ε4 allele of the apolipoprotein E (ApoE) gene, the major apolipoprotein involved in brain cholesterol homeostasis. Being astrocytes the main producers of cholesterol and ApoE in the brain, [...] Read more.
The strongest genetic risk factor for sporadic Alzheimer’s disease (AD) is the presence of the ε4 allele of the apolipoprotein E (ApoE) gene, the major apolipoprotein involved in brain cholesterol homeostasis. Being astrocytes the main producers of cholesterol and ApoE in the brain, we investigated the impact of the ApoE genotype on astrocyte cholesterol homeostasis. Two mouse astrocytic cell lines expressing the human ApoE3 or ApoE4 isoform were employed. Gas chromatography–mass spectrometry (GC-MS) analysis pointed out that the levels of total cholesterol, cholesterol precursors, and various oxysterols are altered in ApoE4 astrocytes. Moreover, the gene expression analysis of more than 40 lipid-related genes by qRT-PCR showed that certain genes are up-regulated (e.g., CYP27A1) and others down-regulated (e.g., PPARγ, LXRα) in ApoE4, compared to ApoE3 astrocytes. Beyond confirming the significant reduction in the levels of PPARγ, a key transcription factor involved in the maintenance of lipid homeostasis, Western blotting showed that both intracellular and secreted ApoE levels are altered in ApoE4 astrocytes, as well as the levels of receptors and transporters involved in lipid uptake/efflux (ABCA1, LDLR, LRP1, and ApoER2). Data showed that the ApoE genotype clearly affects astrocytic cholesterol homeostasis; however, further investigation is needed to clarify the mechanisms underlying these differences and the consequences on neighboring cells. Indeed, drug development aimed at restoring cholesterol homeostasis could be a potential strategy to counteract AD. Full article
(This article belongs to the Special Issue Lipid Metabolism and Redox Regulation in Diseases)
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