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Cells
Special Issues
Focus on Machinery of Cell Death
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Focus on Machinery of Cell Death

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 15 December 2025 | Viewed by 13140

Special Issue Editors

Dr. Subhadip Mukhopadhyay

E-Mail Website1 Website2
Guest Editor
Department of Radiation Oncology, Laura and Isaac Perlmutter Cancer Center, New York University School of Medicine, New York, NY 10016, USA
Interests: cancer; autophagy; apoptosis; cell biology; biochemistry; metabolism; therapy
Dr. Prashanta Kumar Panda

E-Mail Website
Guest Editor
Medical Oncology, Department of Internal Medicine, Washington University School of Medicine in St. Louis, St. Louis, MO, USA
Interests: autophagy; cancer; metabolism; apoptosis; stem cell biology
Dr. Suprabhat Mukherjee

E-Mail Website
Guest Editor
Integrative Biochemistry & Immunology Laboratory, Department of Animal Science, Kazi Nazrul University, West Bengal, India
Interests: vaccine development; immunotherapy; immunopathogenesis; immunoinformatics; antibodies

Special Issue Information

Dear Colleagues,

This Special Issue of Cells will be devoted to exploring the ever-evolving field of the different molecular mechanisms of cell death during development, diseases, and infection. The focus will be on the cross-talk between different types of cell death induction, including apoptosis, autophagy-associated cell death, necrosis, stem cell biology, metabolism, ageing, neurodegeneration, cancer, and infection-associated diseases, to name a few. We are also welcoming papers that highlight different therapeutic methods of cell death induction, particularly those relevant to the treatment of the mentioned situations.

Papers on the different types of death during mammalian cell demise following the recommendations of the Nomenclature Committee on Cell Death (2018) are encouraged. This Special Issue will also cover how the cell death process undergoes developmental transformation and how this makes us more vulnerable with time. On that note, the different dietary and life style changes that can help us ensure a better life will be emphasized, by focusing on the role of antioxidant redox biology in cell death and development.

We hope that this Special Issue will provide a very interesting platform to learn new developments from bench to bedside therapies by enhancing our knowledge around cell death mechanism pathways. Both original research articles and reviews are welcome. 

Dr. Subhadip Mukhopadhyay
Dr. Prashanta Kumar Panda
Dr. Suprabhat Mukherjee
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • cell death
  • autophagy
  • apoptosis
  • necrosis
  • ferroptosis
  • metabolism
  • stem cell biology
  • infection
  • aging
  • development
  • Alzheimer’s
  • neurodegeneration
  • therapy

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Published Papers (6 papers)

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Research

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15 pages, 2615 KiB  
Article
Interleukin 24 Promotes Mitochondrial Dysfunction, Glucose Regulation, and Apoptosis by Inactivating Glycogen Synthase Kinase 3 Beta in Human Prostate Cancer Cells
by Anastassiya Kim, Sual Lopez, Simira Smith, Alphons Sony, Jennifer Abreu, Columba de la Parra and Moira Sauane
Cells 2025, 14(5), 357; https://doi.org/10.3390/cells14050357 - 28 Feb 2025
Viewed by 668
Abstract
Interleukin 24 (IL-24) is a tumor-suppressing protein currently in clinical trials. We previously demonstrated that IL-24 leads to apoptosis in cancer cells through protein kinase A (PKA) activation in human breast cancer cells. To better understand the mechanism by which IL-24 induces apoptosis, [...] Read more.
Interleukin 24 (IL-24) is a tumor-suppressing protein currently in clinical trials. We previously demonstrated that IL-24 leads to apoptosis in cancer cells through protein kinase A (PKA) activation in human breast cancer cells. To better understand the mechanism by which IL-24 induces apoptosis, we analyzed the role of glycogen synthase kinase-3 beta (GSK3β), a highly conserved serine/threonine kinase in cancer cells and a downstream target of PKA. Our studies show for the first time that GSK3β is inhibited following IL-24 treatment in human prostate cancer cells. We showed that the inhibition of GSK3β is mediated through PKA activation triggered by IL-24. IL-24 decreases the phosphorylation of glycogen synthase, substantially activating glycogen synthase and decreasing intracellular glucose levels. Notably, the expression of a constitutively active form of GSK3β abolishes the effect of IL-24. These results demonstrate a previously unrecognized role of IL-24 in apoptosis mediated through GSK3β regulation and its possible implications for metabolic stress, mitochondria dysfunction, and apoptosis. Future studies should precisely delineate the most effective combinations of IL-24 as a GSK3β inhibitor with cytotoxic agents for prostate and other cancers. GSK3β inhibition disrupts average glucose utilization in cancer cells, potentially creating metabolic stress that could be exploited therapeutically. Full article
(This article belongs to the Special Issue Focus on Machinery of Cell Death)
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12 pages, 2279 KiB  
Article
Lactoferrin-Derived Peptide Chimera Induces Caspase-Independent Cell Death in Multiple Myeloma
by Young-Saeng Jang, Shima Barati Dehkohneh, Jaewon Lim, Jaehui Kim, Donghwan Ahn, Sun Shim Choi and Seung Goo Kang
Cells 2025, 14(3), 217; https://doi.org/10.3390/cells14030217 - 3 Feb 2025
Viewed by 1143
Abstract
Lactoferrin-derived peptide chimera is a synthetic peptide that mimics the functional unit of lactoferrin with antibacterial activity. Although LF has anticancer effects, to the best of our knowledge, its effects on multiple myeloma have not yet been studied. We explored the potential of [...] Read more.
Lactoferrin-derived peptide chimera is a synthetic peptide that mimics the functional unit of lactoferrin with antibacterial activity. Although LF has anticancer effects, to the best of our knowledge, its effects on multiple myeloma have not yet been studied. We explored the potential of a lactoferrin-derived chimera for multiple myeloma treatment, a malignant clonal plasma cell bone marrow disease. The lactoferrin-derived chimera effectively inhibited MM1S, MM1R, and RPMI8226 multiple myeloma cell growth, and induced the early and late phases of apoptosis, but not in normal peripheral blood mononuclear cells. Furthermore, the lactoferrin-derived chimera modulates the relative expression of genes involved in survival, apoptosis, and mitochondrial dysfunction at the transcriptional level. Mitochondrial analysis revealed that lactoferrin-derived chimera triggered oxidative stress in multiple myeloma cells, leading to reactive oxygen species generation and a decline in mitochondrial membrane potential, resulting in mitochondrial dysfunction. Although lactoferrin-derived chimera did not cause caspase-dependent cell death, it induced nuclear translocation of apoptosis-inducing factor and endonuclease G, indicating the initiation of caspase-independent apoptosis. Overall, the lactoferrin-derived chimera induces caspase-independent programmed cell death in multiple myeloma cell lines by increasing the nuclear translocation of apoptosis-inducing factor/endonuclease G. Therefore, it has potential for multiple myeloma cancer therapies. Full article
(This article belongs to the Special Issue Focus on Machinery of Cell Death)
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14 pages, 2955 KiB  
Article
The Proteoglycans Biglycan and Decorin Protect Cardiac Cells against Irradiation-Induced Cell Death by Inhibiting Apoptosis
by Renáta Gáspár, Petra Diószegi, Dóra Nógrádi-Halmi, Barbara Erdélyi-Furka, Zoltán Varga, Zsuzsanna Kahán and Tamás Csont
Cells 2024, 13(10), 883; https://doi.org/10.3390/cells13100883 - 20 May 2024
Cited by 1 | Viewed by 1930
Abstract
Radiation-induced heart disease (RIHD), a common side effect of chest irradiation, is a primary cause of mortality among patients surviving thoracic cancer. Thus, the development of novel, clinically applicable cardioprotective agents which can alleviate the harmful effects of irradiation on the heart is [...] Read more.
Radiation-induced heart disease (RIHD), a common side effect of chest irradiation, is a primary cause of mortality among patients surviving thoracic cancer. Thus, the development of novel, clinically applicable cardioprotective agents which can alleviate the harmful effects of irradiation on the heart is of great importance in the field of experimental oncocardiology. Biglycan and decorin are structurally related small leucine-rich proteoglycans which have been reported to exert cardioprotective properties in certain cardiovascular pathologies. Therefore, in the present study we aimed to examine if biglycan or decorin can reduce radiation-induced damage of cardiomyocytes. A single dose of 10 Gray irradiation was applied to induce radiation-induced cell damage in H9c2 cardiomyoblasts, followed by treatment with either biglycan or decorin at various concentrations. Measurement of cell viability revealed that both proteoglycans improved the survival of cardiac cells post-irradiation. The cardiocytoprotective effect of both biglycan and decorin involved the alleviation of radiation-induced proapoptotic mechanisms by retaining the progression of apoptotic membrane blebbing and lowering the number of apoptotic cell nuclei and DNA double-strand breaks. Our findings provide evidence that these natural proteoglycans may exert protection against radiation-induced damage of cardiac cells. Full article
(This article belongs to the Special Issue Focus on Machinery of Cell Death)
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24 pages, 3955 KiB  
Article
β-Catenin Elicits Drp1-Mediated Mitochondrial Fission Activating the Pro-Apoptotic Caspase-1/IL-1β Signalosome in Aeromonas hydrophila-Infected Zebrafish Macrophages
by Shagun Sharma, Manmohan Kumar, Jai Kumar and Shibnath Mazumder
Cells 2023, 12(11), 1509; https://doi.org/10.3390/cells12111509 - 30 May 2023
Cited by 2 | Viewed by 2230
Abstract
Canonical Wnt signaling plays a major role in regulating microbial pathogenesis. However, to date, its involvement in A. hydrophila infection is not well known. Using zebrafish (Danio rerio) kidney macrophages (ZKM), we report that A. hydrophila infection upregulates wnt2, wnt3a [...] Read more.
Canonical Wnt signaling plays a major role in regulating microbial pathogenesis. However, to date, its involvement in A. hydrophila infection is not well known. Using zebrafish (Danio rerio) kidney macrophages (ZKM), we report that A. hydrophila infection upregulates wnt2, wnt3a, fzd5, lrp6, and β-catenin (ctnnb1) expression, coinciding with the decreased expression of gsk3b and axin. Additionally, increased nuclear β-catenin protein accumulation was observed in infected ZKM, thereby suggesting the activation of canonical Wnt signaling in A. hydrophila infection. Our studies with the β-catenin specific inhibitor JW67 demonstrated β-catenin to be pro-apoptotic, which initiates the apoptosis of A. hydrophila-infected ZKM. β-catenin induces NADPH oxidase (NOX)-mediated ROS production, which orchestrates sustained mitochondrial ROS (mtROS) generation in the infected ZKM. Elevated mtROS favors the dissipation of the mitochondrial membrane potential (ΔΨm) and downstream Drp1-mediated mitochondrial fission, leading to cytochrome c release. We also report that β-catenin-induced mitochondrial fission is an upstream regulator of the caspase-1/IL-1β signalosome, which triggers the caspase-3 mediated apoptosis of the ZKM as well as A. hydrophila clearance. This is the first study suggesting a host-centric role of canonical Wnt signaling pathway in A. hydrophila pathogenesis wherein β-catenin plays a primal role in activating the mitochondrial fission machinery, which actively promotes ZKM apoptosis and helps in containing the bacteria. Full article
(This article belongs to the Special Issue Focus on Machinery of Cell Death)
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16 pages, 3276 KiB  
Article
Role of Mitochondrial Iron Overload in Mediating Cell Death in H9c2 Cells
by Eddie Tam, Hye Kyoung Sung, Nhat Hung Lam, Sally You, Sungji Cho, Saher M. Ahmed, Ali A. Abdul-Sater and Gary Sweeney
Cells 2023, 12(1), 118; https://doi.org/10.3390/cells12010118 - 28 Dec 2022
Cited by 14 | Viewed by 4204
Abstract
Iron overload (IO) is associated with cardiovascular diseases, including heart failure. Our study’s aim was to examine the mechanism by which IO triggers cell death in H9c2 cells. IO caused accumulation of intracellular and mitochondrial iron as shown by the use of iron-binding [...] Read more.
Iron overload (IO) is associated with cardiovascular diseases, including heart failure. Our study’s aim was to examine the mechanism by which IO triggers cell death in H9c2 cells. IO caused accumulation of intracellular and mitochondrial iron as shown by the use of iron-binding fluorescent reporters, FerroOrange and MitoFerroFluor. Expression of cytosolic and mitochondrial isoforms of Ferritin was also induced by IO. IO-induced iron accumulation and cellular ROS was rapid and temporally linked. ROS accumulation was detected in the cytosol and mitochondrial compartments with CellROX, DCF-DA and MitoSOX fluorescent dyes and partly reversed by the general antioxidant N-acetyl cysteine or the mitochondrial antioxidant SkQ1. Antioxidants also reduced the downstream activation of apoptosis and lytic cell death quantified by Caspase 3 cleavage/activation, mitochondrial Cytochrome c release, Annexin V/Propidium iodide staining and LDH release of IO-treated cells. Finally, overexpression of MitoNEET, an outer mitochondrial membrane protein involved in the transfer of Fe-S clusters between mitochondrial and cytosol, was observed to lower iron and ROS accumulation in the mitochondria. These alterations were correlated with reduced IO-induced cell death by apoptosis in MitoNEET-overexpressing cells. In conclusion, IO mediates H9c2 cell death by causing mitochondrial iron accumulation and subsequent general and mitochondrial ROS upregulation. Full article
(This article belongs to the Special Issue Focus on Machinery of Cell Death)
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Review

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17 pages, 2035 KiB  
Review
Methuosis, Alkaliptosis, and Oxeiptosis and Their Significance in Anticancer Therapy
by Elżbieta Bartoszewska, Kamila Florek, Karol Zagórski, Martyna Gachowska, Anna Wietrzyk, Agata Hutny, Agnieszka Nowakowska-Toporowska and Julita Kulbacka
Cells 2024, 13(24), 2095; https://doi.org/10.3390/cells13242095 - 18 Dec 2024
Cited by 1 | Viewed by 1341
Abstract
Understanding morphological, biochemical, and functional aspects of cell death is essential for targeting new cancer therapies. Even though many different mechanisms of cell death are identified, it is crucial to highlight the role of new and lesser-known pathways, including methuosis, alkaliptosis, and oxeiptosis. [...] Read more.
Understanding morphological, biochemical, and functional aspects of cell death is essential for targeting new cancer therapies. Even though many different mechanisms of cell death are identified, it is crucial to highlight the role of new and lesser-known pathways, including methuosis, alkaliptosis, and oxeiptosis. The aim of this review was to summarize the data about cell death mechanisms—methuosis, alkaliptosis, and oxeiptosis—and their role in cancer treatment. Unique molecular mechanisms and cellular outcomes characterize each of these forms of cell death. This research on methuosis, alkaliptosis, and oxeiptosis provides a better understating of cell death biology and creates novel opportunities for neoplasm management. Full article
(This article belongs to the Special Issue Focus on Machinery of Cell Death)
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