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Programmed Cell Death and Oxidative Stress 2.0
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Programmed Cell Death and Oxidative Stress 2.0

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

Deadline for manuscript submissions: 30 May 2024 | Viewed by 4413

Special Issue Editor

Dr. Takuya Noguchi

E-Mail Website
Guest Editor
Department of Biopharmaceutical Science, Tohoku University, Sendai 980-8578, Japan
Interests: apoptosis; signaling pathways; phosphorylation; signal transduction; cell signaling; reactive oxygen species; molecular cell biology; cell biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

This Special Issue is a continuation of our previous Special Issue “Programmed Cell Death and Oxidative Stress”.

Cells that constitute aerobic organisms are continuously exposed to reactive oxygen species (ROS), whose accumulation often initiates oxidative stress. Importantly, oxidative stress plays a critical role in the determination of cell fate by inducing cellular responses, such as proliferation, differentiation, and programmed cell death. Accumulating evidence indicates that oxidative stress initiates various forms of programmed cell death including apoptosis, necroptosis, pyroptosis, parthanatos, and ferroptosis. Moreover, all types of oxidative-stress-induced cell death are closely associated with a wide variety of diseases. For this Special Issue, studies of a wide range of signaling mechanisms and pathological processes related to oxidative stress-induced cell death are welcome.

Dr. Takuya Noguchi
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.

Keywords

  • oxidative stress
  • programmed cell death
  • cellular stresses
  • senescence
  • cytotoxicity
  • cancer
  • neurodegenerative disease
  • inflammatory disease
  • organelle stress

Related Special Issue

Published Papers (6 papers)

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Research

23 pages, 6150 KiB  
Article
Mechanisms of PM10 Disruption of the Nrf2 Pathway in Cornea
by Mallika Somayajulu, Farooq S. Muhammed, Robert Wright, Sharon A. McClellan and Linda D. Hazlett
Int. J. Mol. Sci. 2024, 25(7), 3754; https://doi.org/10.3390/ijms25073754 - 28 Mar 2024
Viewed by 434
Abstract
We have previously shown that PM10 exposure causes oxidative stress and reduces Nrf2 protein levels, and SKQ1 pre-treatment protects against this damage in human corneal epithelial cells (HCE-2). The current study focuses on uncovering the mechanisms underlying acute PM10 toxicity and [...] Read more.
We have previously shown that PM10 exposure causes oxidative stress and reduces Nrf2 protein levels, and SKQ1 pre-treatment protects against this damage in human corneal epithelial cells (HCE-2). The current study focuses on uncovering the mechanisms underlying acute PM10 toxicity and SKQ1-mediated protection. HCE-2 were pre-treated with SKQ1 and then exposed to 100 μg/mL PM10. Cell viability, oxidative stress markers, programmed cell death, DNA damage, senescence markers, and pro-inflammatory cytokines were analyzed. Nrf2 cellular location and its transcriptional activity were determined. Effects of the Nrf2 inhibitor ML385 were similarly evaluated. Data showed that PM10 decreased cell viability, Nrf2 transcriptional activity, and mRNA levels of antioxidant enzymes, but increased p-PI3K, p-NFκB, COX-2, and iNOS proteins levels. Additionally, PM10 exposure significantly increased DNA damage, phosphor-p53, p16 and p21 protein levels, and β-galactosidase (β-gal) staining, which confirmed the senescence. SKQ1 pre-treatment reversed these effects. ML385 lowered the Nrf2 protein levels and mRNA levels of its downstream targets. ML385 also abrogated the protective effects of SKQ1 against PM10 toxicity by preventing the restoration of cell viability and reduced oxidative stress. In conclusion, PM10 induces inflammation, reduces Nrf2 transcriptional activity, and causes DNA damage, leading to a senescence-like phenotype, which is prevented by SKQ1. Full article
(This article belongs to the Special Issue Programmed Cell Death and Oxidative Stress 2.0)
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17 pages, 3674 KiB  
Article
Involvement of Ferroptosis Induction and Oxidative Phosphorylation Inhibition in the Anticancer-Drug-Induced Myocardial Injury: Ameliorative Role of Pterostilbene
by Kiyomu Fujii, Rina Fujiwara-Tani, Shota Nukaga, Hitoshi Ohmori, Yi Luo, Ryoichi Nishida, Takamitsu Sasaki, Yoshihiro Miyagawa, Chie Nakashima, Isao Kawahara, Ruiko Ogata, Ayaka Ikemoto, Rika Sasaki and Hiroki Kuniyasu
Int. J. Mol. Sci. 2024, 25(5), 3015; https://doi.org/10.3390/ijms25053015 - 05 Mar 2024
Viewed by 638
Abstract
Patients with cancer die from cardiac dysfunction second only to the disease itself. Cardiotoxicity caused by anticancer drugs has been emphasized as a possible cause; however, the details remain unclear. To investigate this mechanism, we treated rat cardiomyoblast H9c2 cells with sunitinib, lapatinib, [...] Read more.
Patients with cancer die from cardiac dysfunction second only to the disease itself. Cardiotoxicity caused by anticancer drugs has been emphasized as a possible cause; however, the details remain unclear. To investigate this mechanism, we treated rat cardiomyoblast H9c2 cells with sunitinib, lapatinib, 5-fluorouracil, and cisplatin to examine their effects. All anticancer drugs increased ROS, lipid peroxide, and iron (II) levels in the mitochondria and decreased glutathione peroxidase-4 levels and the GSH/GSSG ratio. Against this background, mitochondrial iron (II) accumulates through the unregulated expression of haem oxygenase-1 and ferrochelatase. Anticancer-drug-induced cell death was suppressed by N-acetylcysteine, deferoxamine, and ferrostatin, indicating ferroptosis. Anticancer drug treatment impairs mitochondrial DNA and inhibits oxidative phosphorylation in H9c2 cells. Similar results were observed in the hearts of cancer-free rats treated with anticancer drugs in vitro. In contrast, treatment with pterostilbene inhibited the induction of ferroptosis and rescued the energy restriction induced by anticancer drugs both in vitro and in vivo. These findings suggest that induction of ferroptosis and inhibition of oxidative phosphorylation are mechanisms by which anticancer drugs cause myocardial damage. As pterostilbene ameliorates these mechanisms, it is expected to have significant clinical applications. Full article
(This article belongs to the Special Issue Programmed Cell Death and Oxidative Stress 2.0)
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15 pages, 4335 KiB  
Article
Del-1 Plays a Protective Role against COPD Development by Inhibiting Inflammation and Apoptosis
by Nakwon Kwak, Kyoung-Hee Lee, Jisu Woo, Jiyeon Kim, Jimyung Park, Chang-Hoon Lee and Chul-Gyu Yoo
Int. J. Mol. Sci. 2024, 25(4), 1955; https://doi.org/10.3390/ijms25041955 - 06 Feb 2024
Viewed by 657
Abstract
Neutrophilic inflammation is a prominent feature of chronic obstructive pulmonary disease (COPD). Developmental endothelial locus-1 (Del-1) has been reported to limit excessive neutrophilic inflammation by inhibiting neutrophil adhesion to the vascular endothelial cells. However, the effects of Del-1 in COPD are not known. [...] Read more.
Neutrophilic inflammation is a prominent feature of chronic obstructive pulmonary disease (COPD). Developmental endothelial locus-1 (Del-1) has been reported to limit excessive neutrophilic inflammation by inhibiting neutrophil adhesion to the vascular endothelial cells. However, the effects of Del-1 in COPD are not known. We investigated the role of Del-1 in the pathogenesis of COPD. Del-1 protein expression was decreased in the lungs of COPD patients, especially in epithelial cells and alveolar macrophages. In contrast to human lung tissue, Del-1 expression was upregulated in lung tissue from mice treated with cigarette smoke extracts (CSE). Overexpression of Del-1 significantly suppressed IL-8 release and apoptosis in CSE-treated epithelial cells. In contrast, knockdown of Del-1 enhanced IL-8 release and apoptosis. In macrophages, overexpression of Del-1 significantly suppressed inflammatory cytokine release, and knockdown of Del-1 enhanced it. This anti-inflammatory effect was mediated by inhibiting the phosphorylation and acetylation of NF-κB p65. Nuclear factor erythroid 2-related factor 2 (Nrf2) activators, such as quercetin, resveratrol, and sulforaphane, increased Del-1 in both cell types. These results suggest that Del-1, mediated by Nrf2, plays a protective role against the pathogenesis of COPD, at least in part through anti-inflammatory and anti-apoptotic effects. Full article
(This article belongs to the Special Issue Programmed Cell Death and Oxidative Stress 2.0)
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12 pages, 1396 KiB  
Communication
Cumulative Deleterious Effects of Tetrahydrocannabinoid (THC) and Ethanol on Mitochondrial Respiration and Reactive Oxygen Species Production Are Enhanced in Old Isolated Cardiac Mitochondria
by Anne-Laure Charles, Anne Charloux, Thomas Vogel, Jean-Sébastien Raul, Michel Kindo, Valérie Wolff and Bernard Geny
Int. J. Mol. Sci. 2024, 25(3), 1835; https://doi.org/10.3390/ijms25031835 - 02 Feb 2024
Cited by 1 | Viewed by 774
Abstract
Delta 9 tetrahydrocannabinol (THC), the main component of cannabis, has adverse effects on the cardiovascular system, but whether concomitant ethanol (EtOH) and aging modulate its toxicity is unknown. We investigated dose responses of THC and its vehicle, EtOH, on mitochondrial respiration and reactive [...] Read more.
Delta 9 tetrahydrocannabinol (THC), the main component of cannabis, has adverse effects on the cardiovascular system, but whether concomitant ethanol (EtOH) and aging modulate its toxicity is unknown. We investigated dose responses of THC and its vehicle, EtOH, on mitochondrial respiration and reactive oxygen production in both young and old rat cardiac mitochondria (12 and 90 weeks). THC dose-dependently impaired mitochondrial respiration in both groups, and such impairment was enhanced in aged rats (−97.5 ± 1.4% vs. −75.6 ± 4.0% at 2 × 10−5 M, and IC50: 0.7 ± 0.05 vs. 1.3 ± 0.1 × 10−5 M, p < 0.01, for old and young rats, respectively). The EtOH-induced decrease in mitochondrial respiration was greater in old rats (−50.1 ± 2.4% vs. −19.8 ± 4.4% at 0.9 × 10−5 M, p < 0.0001). Further, mitochondrial hydrogen peroxide (H2O2) production was enhanced in old rats after THC injection (+46.6 ± 5.3 vs. + 17.9 ± 7.8%, p < 0.01, at 2 × 10−5 M). In conclusion, the deleterious cardiac effects of THC were enhanced with concomitant EtOH, particularly in old cardiac mitochondria, showing greater mitochondrial respiration impairment and ROS production. These data improve our knowledge of the mechanisms potentially involved in cannabis toxicity, and likely support additional caution when THC is used by elderly people who consume alcohol. Full article
(This article belongs to the Special Issue Programmed Cell Death and Oxidative Stress 2.0)
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13 pages, 3023 KiB  
Article
Unravelling the Transcriptional Response of Agaricus bisporus under Lecanicillium fungicola Infection
by Luis Felipe Quiroz, Tessa Ciosek, Helen Grogan, Peter C. McKeown, Charles Spillane and Galina Brychkova
Int. J. Mol. Sci. 2024, 25(2), 1283; https://doi.org/10.3390/ijms25021283 - 20 Jan 2024
Viewed by 814
Abstract
Mushrooms are a nutritionally rich and sustainably-produced food with a growing global market. Agaricus bisporus accounts for 11% of the total world mushroom production and it is the dominant species cultivated in Europe. It faces threats from pathogens that cause important production losses, [...] Read more.
Mushrooms are a nutritionally rich and sustainably-produced food with a growing global market. Agaricus bisporus accounts for 11% of the total world mushroom production and it is the dominant species cultivated in Europe. It faces threats from pathogens that cause important production losses, including the mycoparasite Lecanicillium fungicola, the causative agent of dry bubble disease. Through quantitative real-time polymerase chain reaction (qRT-PCR), we determine the impact of L. fungicola infection on the transcription patterns of A. bisporus genes involved in key cellular processes. Notably, genes related to cell division, fruiting body development, and apoptosis exhibit dynamic transcriptional changes in response to infection. Furthermore, A. bisporus infected with L. fungicola were found to accumulate increased levels of reactive oxygen species (ROS). Interestingly, the transcription levels of genes involved in the production and scavenging mechanisms of ROS were also increased, suggesting the involvement of changes to ROS homeostasis in response to L. fungicola infection. These findings identify potential links between enhanced cell proliferation, impaired fruiting body development, and ROS-mediated defence strategies during the A. bisporus (host)–L. fungicola (pathogen) interaction, and offer avenues for innovative disease control strategies and improved understanding of fungal pathogenesis. Full article
(This article belongs to the Special Issue Programmed Cell Death and Oxidative Stress 2.0)
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13 pages, 1825 KiB  
Article
Neuroprotective Effects of Noncanonical PAR1 Agonists on Cultured Neurons in Excitotoxicity
by Irina Babkina, Irina Savinkova, Tatiana Molchanova, Maria Sidorova, Alexander Surin and Liubov Gorbacheva
Int. J. Mol. Sci. 2024, 25(2), 1221; https://doi.org/10.3390/ijms25021221 - 19 Jan 2024
Viewed by 590
Abstract
Serine proteases regulate cell functions through G protein-coupled protease-activated receptors (PARs). Cleavage of one peptide bond of the receptor amino terminus results in the formation of a new N-terminus (“tethered ligand”) that can specifically interact with the second extracellular loop of the PAR [...] Read more.
Serine proteases regulate cell functions through G protein-coupled protease-activated receptors (PARs). Cleavage of one peptide bond of the receptor amino terminus results in the formation of a new N-terminus (“tethered ligand”) that can specifically interact with the second extracellular loop of the PAR receptor and activate it. Activation of PAR1 by thrombin (canonical agonist) and activated protein C (APC, noncanonical agonist) was described as a biased agonism. Here, we have supposed that synthetic peptide analogs to the PAR1 tethered ligand liberated by APC could have neuroprotective effects like APC. To verify this hypothesis, a model of the ischemic brain impairment based on glutamate (Glu) excitotoxicity in primary neuronal cultures of neonatal rats has been used. It was shown that the nanopeptide NPNDKYEPF-NH2 (AP9) effectively reduced the neuronal death induced by Glu. The influence of AP9 on cell survival was comparable to that of APC. Both APC and AP9 reduced the dysregulation of intracellular calcium homeostasis in cultured neurons induced by excitotoxic Glu (100 µM) or NMDA (200 µM) concentrations. PAR1 agonist synthetic peptides might be noncanonical PAR1 agonists and a basis for novel neuroprotective drugs for disorders related to Glu excitotoxicity such as brain ischemia, trauma and some neurodegenerative diseases. Full article
(This article belongs to the Special Issue Programmed Cell Death and Oxidative Stress 2.0)
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