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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 8164

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 (3 papers)

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Research

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
Viewed by 1365
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 1928
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 13 | Viewed by 3634
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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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Novel Insights into the Mechanisms of Pro-Apoptotic TRAIL Receptor Activation
Authors: Law,Brian K.; Law,Mary Elizabeth
Affiliation: 1
Abstract: TNF-related apoptosis-inducing ligand/Apo-2 ligand (TRAIL) was discovered long ago to selectively induce apoptosis of cancer cells through Death Receptors 4 and 5 (DR4/5), while sparing normal tissue. Despite the important role of TRAIL in anti-cancer immunity and metastasis suppression, and the safety of TRAIL analogs and agonistic antibodies, agents targeting the TRAIL/TRAIL receptor pathway have shown insufficient anti-cancer efficacy in unstratified patients in clinical trials. This review briefly outlines the TRAIL/TRAIL receptor pro-apoptotic signaling pathway, cross-species differences in TRAIL signaling, mechanisms of TRAIL resistance, and pharmacological liabilities of TRAIL analogs and TRAIL receptor agonistic antibodies. The remainder of the review focuses on 1) the mechanisms responsible for TRAIL selectivity for cancer cells, 2) the recent discovery of and mechanistic insights into an extracellular DR5 auto-inhibitory domain, and 3) how the new conceptual model for DR5 activation may a) explain how DR5 functions as a direct receptor for misfolded proteins, b) predict the anti-cancer efficacy of DR5 agonist antibodies, and c) reveal differential disulfide bonding as a molecular “switch” between active and inactive DR5 conformations.

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