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Special Issue "Cellular Redox Mechanisms in Inflammation and Programmed Cell Death"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 1 March 2024 | Viewed by 1012

Special Issue Editor

Institute for Regenerative Medicine, Sechenov First Moscow State Medical University, 119435 Moscow, Russia
Interests: innate immunity; neutrophils; macrophages; reactive oxygen species; peroxidases

Special Issue Information

Dear Colleagues,

Redox reactions play an important role in the regulation of physiological processes. Cellular redox balance can vary widely dependently on cell activity and homeostatic capacity, as well as exposure to stress factors. Normally, redox reactions are strictly controlled; however, during inflammation and programmed cell death (e.g., apoptosis and ferroptosis), increased oxidant production and redox dysregulation contribute to cell injury, culminating in cell demise. Even in these extreme conditions, there are regulatory factors that control the poorly balanced redox processes and limit the spreading of cell death and tissue damage. Notably, inflammatory responses and cell death programs include three stages: initiation, progression, and termination (or cell removal). At all stages, reactive oxygen species and redox enzymes are the key players in the regulation of physiological processes.

The research topics of this Special Issue on redox mechanisms involved in the regulation of inflammation and programmed forms of cell death include the following:

  • The radical-generating activity of neutrophils and macrophages in the initiation stage of inflammation.
  • The enzymatically controlled production and dismutation of redox-active molecules: NADPH-oxidase (and other Nox), myeloperoxidase, superoxide dismutases, etc.
  • The iron-dependent oxidation of cellular lipids and the synthesis of lipid mediators.
  • NO• as a regulator of inflammation and cell death.
  • Enzymatic and non-enzymatic antioxidants that contribute to the suppression of oxidative stress (thioredoxin family proteins, glutathione peroxidases/reductases, etc.)
  • Redox signaling aimed at the removal of dead and damaged cells, and phagocyte redox-activity.

We welcome the submission of research reports, reviews, and mini-reviews that are within the scope of these subjects.

Dr. Irina I. Vlasova
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.


  • neutrophils
  • macrophages
  • reactive oxygen species
  • nitric oxide
  • redox-active enzymes
  • lipid oxidation
  • inflammatory response
  • apoptosis
  • ferroptosis

Published Papers (1 paper)

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Inhibition of Ferroptosis Enables Safe Rewarming of HEK293 Cells following Cooling in University of Wisconsin Cold Storage Solution
Int. J. Mol. Sci. 2023, 24(13), 10939; https://doi.org/10.3390/ijms241310939 - 30 Jun 2023
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The prolonged cooling of cells results in cell death, in which both apoptosis and ferroptosis have been implicated. Preservation solutions such as the University of Wisconsin Cold Storage Solution (UW) encompass approaches addressing both. The use of UW improves survival and thus extends [...] Read more.
The prolonged cooling of cells results in cell death, in which both apoptosis and ferroptosis have been implicated. Preservation solutions such as the University of Wisconsin Cold Storage Solution (UW) encompass approaches addressing both. The use of UW improves survival and thus extends preservation limits, yet it remains unclear how exactly organ preservation solutions exert their cold protection. Thus, we explored cooling effects on lipid peroxidation and adenosine triphosphate (ATP) levels and the actions of blockers of apoptosis and ferroptosis, and of compounds enhancing mitochondrial function. Cooling and rewarming experiments were performed in a cellular transplantation model using Human Embryonic Kidney (HEK) 293 cells. Cell viability was assessed by neutral red assay. Lipid peroxidation levels were measured by Western blot against 4-Hydroxy-Nonenal (4HNE) and the determination of Malondialdehyde (MDA). ATP was measured by luciferase assay. Cooling beyond 5 h in Dulbecco’s Modified Eagle Medium (DMEM) induced complete cell death in HEK293, whereas cooling in UW preserved ~60% of the cells, with a gradual decline afterwards. Cooling-induced cell death was not precluded by inhibiting apoptosis. In contrast, the blocking of ferroptosis by Ferrostatin-1 or maintaining of mitochondrial function by the 6-chromanol SUL150 completely inhibited cell death both in DMEM- and UW-cooled cells. Cooling for 24 h in UW followed by rewarming for 15 min induced a ~50% increase in MDA, while concomitantly lowering ATP by >90%. Treatment with SUL150 of cooled and rewarmed HEK293 effectively precluded the increase in MDA and preserved normal ATP in both DMEM- and UW-cooled cells. Likewise, treatment with Ferrostatin-1 blocked the MDA increase and preserved the ATP of rewarmed UW HEK293 cells. Cooling-induced HEK293 cell death from hypothermia and/or rewarming was caused by ferroptosis rather than apoptosis. UW slowed down ferroptosis during hypothermia, but lipid peroxidation and ATP depletion rapidly ensued upon rewarming, ultimately resulting in complete cell death. Treatment throughout UW cooling with small-molecule Ferrostatin-1 or the 6-chromanol SUL150 effectively prevented ferroptosis, maintained ATP, and limited lipid peroxidation in UW-cooled cells. Counteracting ferroptosis during cooling in UW-based preservation solutions may provide a simple method to improve graft survival following cold static cooling. Full article
(This article belongs to the Special Issue Cellular Redox Mechanisms in Inflammation and Programmed Cell Death)
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