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Antioxidants
Special Issues
Crosstalk between Autophagy and Oxidative Stress
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Crosstalk between Autophagy and Oxidative Stress

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: 31 December 2024 | Viewed by 1476

Special Issue Editors

Dr. Marina Garcia-Macia

E-Mail Website
Guest Editor
Institute of Biomedical Research of Salamanca, University Hospital of Salamanca, 37007 Salamanca, Spain
Interests: oxidative stress; autophagy; lipophagy; metabolism; neuroscience; liver; metabolic diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Álvaro F. Fernández

E-Mail Website
Guest Editor
1. Instituto de Investigación Sanitaria del Principado de Asturias, 33011 Oviedo, Spain
2. Departamento de Biología Funcional, Universidad de Oviedo, 33011 Oviedo, Spain
Interests: autophagy; aging; animal models; metabolism; cell death
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autophagy, a fundamental cellular mechanism, plays a pivotal role in maintaining cellular homeostasis by facilitating the removal of damaged organelles and proteins. Autophagy can be activated in response to various stressors, such as nutrient deprivation, hypoxia, drugs, and virus-mediated infections. More and more evidence in recent years indicates that autophagy is a crucial mediator in the regulation of oxidative stress response.

This Special Issue aims to provide a comprehensive platform for researchers to delve into the cross-regulation between autophagy and oxidative stress. Topics will encompass the molecular mechanisms governing this crosstalk, its impact on cellular functions, and the implications for various diseases, including neurodegenerative disorders, cancer, and metabolic diseases.

We invite contributions from experts across disciplines to explore the latest advancements in understanding how autophagy and oxidative stress communicate within cellular environments. By fostering collaborative discussions, this Special Issue seeks to deepen our insights into these interconnected processes, paving the way for innovative therapeutic strategies and unveiling novel targets for intervention.

Dr. Marina Garcia-Macia
Dr. Álvaro F. Fernández
Guest Editors

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

  • autophagy
  • oxidative stress
  • reactive oxygen species
  • aging
  • cellular homeostasis

Published Papers (2 papers)

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Research

21 pages, 18370 KiB  
Article
Luteolin Alleviates Cadmium-Induced Kidney Injury by Inhibiting Oxidative DNA Damage and Repairing Autophagic Flux Blockade in Chickens
by Kanglei Zhang, Jiahui Li, Wenxuan Dong, Qing Huang, Xueru Wang, Kai Deng, Waseem Ali, Ruilong Song, Hui Zou, Di Ran, Gang Liu and Zongping Liu
Antioxidants 2024, 13(5), 525; https://doi.org/10.3390/antiox13050525 (registering DOI) - 26 Apr 2024
Viewed by 240
Abstract
Chickens are a major source of meat and eggs in human food and have significant economic value. Cadmium (Cd) is a common environmental pollutant that can contaminate feed and drinking water, leading to kidney injury in livestock and poultry, primarily by inducing the [...] Read more.
Chickens are a major source of meat and eggs in human food and have significant economic value. Cadmium (Cd) is a common environmental pollutant that can contaminate feed and drinking water, leading to kidney injury in livestock and poultry, primarily by inducing the generation of free radicals. It is necessary to develop potential medicines to prevent and treat Cd-induced nephrotoxicity in poultry. Luteolin (Lut) is a natural flavonoid compound mainly extracted from peanut shells and has a variety of biological functions to defend against oxidative damage. In this study, we aimed to demonstrate whether Lut can alleviate kidney injury under Cd exposure and elucidate the underlying molecular mechanisms. Renal histopathology and cell morphology were observed. The indicators of renal function, oxidative stress, DNA damage and repair, NAD+ content, SIRT1 activity, and autophagy were analyzed. In vitro data showed that Cd exposure increased ROS levels and induced oxidative DNA damage and repair, as indicated by increased 8-OHdG content, increased γ-H2AX protein expression, and the over-activation of the DNA repair enzyme PARP-1. Cd exposure decreased NAD+ content and SIRT1 activity and increased LC3 II, ATG5, and particularly p62 protein expression. In addition, Cd-induced oxidative DNA damage resulted in PARP-1 over-activation, reduced SIRT1 activity, and autophagic flux blockade, as evidenced by reactive oxygen species scavenger NAC application. The inhibition of PARP-1 activation with the pharmacological inhibitor PJ34 restored NAD+ content and SIRT1 activity. The activation of SIRT1 with the pharmacological activator RSV reversed Cd-induced autophagic flux blockade and cell injury. In vivo data demonstrated that Cd treatment caused the microstructural disruption of renal tissues, reduced creatinine, and urea nitrogen clearance, raised MDA content, and decreased the activities or contents of antioxidants (GSH, T-SOD, CAT, and T-AOC). Cd treatment caused oxidative DNA damage and PARP-1 activation, decreased NAD+ content, decreased SIRT1 activity, and impaired autophagic flux. Notably, the dietary Lut supplement observably alleviated these alterations in chicken kidney tissues induced by Cd. In conclusion, the dietary Lut supplement alleviated Cd-induced chicken kidney injury through its potent antioxidant properties by relieving the oxidative DNA damage-activated PARP-1-mediated reduction in SIRT1 activity and repairing autophagic flux blockade. Full article
(This article belongs to the Special Issue Crosstalk between Autophagy and Oxidative Stress)
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19 pages, 12143 KiB  
Article
Antioxidative Sirt1 and the Keap1-Nrf2 Signaling Pathway Impair Inflammation and Positively Regulate Autophagy in Murine Mammary Epithelial Cells or Mammary Glands Infected with Streptococcus uberis
by Sohrab Khan, Tian Wang, Eduardo R. Cobo, Bingchun Liang, Muhammad Asfandyar Khan, Maolin Xu, Weijie Qu, Jian Gao, Herman W. Barkema, John P. Kastelic, Gang Liu and Bo Han
Antioxidants 2024, 13(2), 171; https://doi.org/10.3390/antiox13020171 - 29 Jan 2024
Viewed by 946
Abstract
Streptococcus uberis mastitis in cattle infects mammary epithelial cells. Although oxidative responses often remove intracellular microbes, S. uberis survives, but the mechanisms are not well understood. Herein, we aimed to elucidate antioxidative mechanisms during pathogenesis of S. uberis after isolation from clinical bovine [...] Read more.
Streptococcus uberis mastitis in cattle infects mammary epithelial cells. Although oxidative responses often remove intracellular microbes, S. uberis survives, but the mechanisms are not well understood. Herein, we aimed to elucidate antioxidative mechanisms during pathogenesis of S. uberis after isolation from clinical bovine mastitis milk samples. S. uberis’s in vitro pathomorphology, oxidative stress biological activities, transcription of antioxidative factors, inflammatory response cytokines, autophagosome and autophagy functions were evaluated, and in vivo S. uberis was injected into the fourth mammary gland nipple of each mouse to assess the infectiousness of S. uberis potential molecular mechanisms. The results showed that infection with S. uberis induced early oxidative stress and increased reactive oxygen species (ROS). However, over time, ROS concentrations decreased due to increased antioxidative activity, including total superoxide dismutase (T-SOD) and malondialdehyde (MDA) enzymes, plus transcription of antioxidative factors (Sirt1, Keap1, Nrf2, HO-1). Treatment with a ROS scavenger (N-acetyl cysteine, NAC) before infection with S. uberis reduced antioxidative responses and the inflammatory response, including the cytokines IL-6 and TNF-α, and the formation of the Atg5-LC3II/LC3I autophagosome. Synthesis of antioxidants determined autophagy functions, with Sirt1/Nrf2 activating autophagy in the presence of S. uberis. This study demonstrated the evasive mechanisms of S. uberis in mastitis, including suppressing inflammatory and ROS defenses by stimulating antioxidative pathways. Full article
(This article belongs to the Special Issue Crosstalk between Autophagy and Oxidative Stress)
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