Oxidative Stress in Ischemia–Reperfusion Injury
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 June 2024 | Viewed by 348
Special Issue Editors
Interests: solid organ transplantation; ischemia–reperfusion injury; extracorporeal machine perfusion; transplantation; medicine; surgery
Interests: solid organ transplantation; ischemia–reperfusion injury; mitochondrial dysfunction; reactive oxygen and nitrogen species; extracorporeal machine perfusion; surgery
Special Issue Information
Dear Colleagues,
Ischemia–reperfusion injury (IRI) is a mechanism that occurs when blood supply to a particular organ or tissue is disrupted, leading to a period of oxygen deprivation. The injury can occur in various pathological conditions, such as myocardial infarction, stroke, trauma and during medical procedures, e.g., solid organ transplantation. Once the blood supply is restored, a sudden surge of oxygen and nutrients leads to a dysregulation of reactive oxygen and nitrogen species (RONS) and other free radicals, leading to oxidative stress and secondary tissue damage. Oxidative stress triggers the activation of various cell death pathways, including apoptosis and necrosis. Additionally, it can exacerbate inflammatory responses, leading to further tissue damage.
The central role of oxidative stress in IRI has led to a significant research effort to identify potential therapeutic targets to mitigate its effects. Antioxidants, such as vitamin E, vitamin C and glutathione, have been investigated as potential therapeutic agents to modulate RONS and reduce oxidative and nitrosative stress. However, the complex machinery of inflammatory pathways and cellular oxidative signalling requires further research.
We are inviting researchers to submit their original research or review articles that may cover a range of topics related to the mechanisms underlying oxidative stress in ischemia–reperfusion injury, as well as potential therapeutic strategies to mitigate its effects. Some of the key themes that can be explored include the role of mitochondrial dysfunction, inflammation and cell death pathways in promoting oxidative stress, as well as the potential protective effects of various antioxidants and other therapeutic agents.
Prof. Dr. Stefan Schneeberger
Dr. Andras Tamas Meszaros
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
- ischemia–reperfusion injury
- oxidative stress
- reactive oxygen and nitrogen species
- free radicals
- antioxidants
- mitochondrial dysfunction
- inflammation
- cell death
- therapeutic strategies
- organ transplantation
