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Cells
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Cell Death in Health and Disease
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Cell Death in Health and Disease

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

Deadline for manuscript submissions: closed (15 August 2023) | Viewed by 13600

Special Issue Editor

Prof. Dr. Jung-Hye Choi

E-Mail Website
Guest Editor
College of Pharmacy, Kyung Hee University, Seoul 02447, Republic of Korea
Interests: ovarian cancer; endometriosis; pharmaceutical science; inflammation; natural product; tumor microenvironment; chemoresistance; apoptosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cell death is the ultimate and irreversible fate for cells and plays an essential role in all aspects of life. It is required for successful embryonic development and the maintenance of normal tissue and immune homeostasis. Moreover, most diseases are associated with deregulated cell death in some way. For example, the evasion of death is one of the hallmarks of cancer. The aberrant activation of cell death signaling is a common feature in neurodegenerative disorders, such as Alzheimer’s disease and amyotrophic lateral sclerosis. Studies over the past several decades have explored the role of various forms of cell death (apoptosis, necroptosis, pyroptosis, and ferroptosis) in human health and diseases and their underlying molecular mechanism. There is growing interest in targeted cell death-based treatment for various human diseases.

This Special Issue of Cells will focus on the role of cell death in major human diseases, including cancer, infectious diseases, and neurodegenerative diseases, as well as approaches to modulate cell death for the treatment of the diseases. This Special Issue welcomes original research articles and review manuscripts.   

Prof. Dr. Jung-Hye Choi
Guest Editor

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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

  • programmed cell death
  • apoptosis
  • cancer
  • neurodegenerative diseases
  • experimental medicine
  • pharmaceutical science

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Published Papers (6 papers)

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Research

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19 pages, 4927 KiB  
Article
Role of the YAP/TAZ-TEAD Transcriptional Complex in the Metabolic Control of TRAIL Sensitivity by the Mevalonate Pathway in Cancer Cells
by Younes El Yousfi, Rocío Mora-Molina, Abelardo López-Rivas and Rosario Yerbes
Cells 2023, 12(19), 2370; https://doi.org/10.3390/cells12192370 - 27 Sep 2023
Cited by 1 | Viewed by 1648
Abstract
Different studies have reported that inhibiting the mevalonate pathway with statins may increase the sensitivity of cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), although the signaling mechanism leading to this sensitization remains largely unknown. We investigated the role of the YAP [...] Read more.
Different studies have reported that inhibiting the mevalonate pathway with statins may increase the sensitivity of cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), although the signaling mechanism leading to this sensitization remains largely unknown. We investigated the role of the YAP (Yes-associated protein)/TAZ (transcriptional co-activator with PDZ-binding motif)-TEAD (TEA/ATTS domain) transcriptional complex in the metabolic control of TRAIL sensitivity by the mevalonate pathway. We show that depleting nuclear YAP/TAZ in tumor cells, either via treatment with statins or by silencing YAP/TAZ expression with siRNAs, facilitates the activation of apoptosis by TRAIL. Furthermore, the blockage of TEAD transcriptional activity either pharmacologically or through the ectopic expression of a disruptor of the YAP/TAZ interaction with TEAD transcription factors, overcomes the resistance of tumor cells to the induction of apoptosis by TRAIL. Our results show that the mevalonate pathway controls cellular the FLICE-inhibitory protein (cFLIP) expression in tumor cells. Importantly, inhibiting the YAP/TAZ-TEAD signaling pathway induces cFLIP down-regulation, leading to a marked sensitization of tumor cells to apoptosis induction by TRAIL. Our data suggest that a combined strategy of targeting TEAD activity and selectively activating apoptosis signaling by agonists of apoptotic TRAIL receptors could be explored as a potential therapeutic approach in cancer treatment. Full article
(This article belongs to the Special Issue Cell Death in Health and Disease)
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13 pages, 2693 KiB  
Article
Novel Variant in CEP250 Causes Protein Mislocalization and Leads to Nonsyndromic Autosomal Recessive Type of Progressive Hearing Loss
by Minjin Kang, Jung Ah Kim, Mee Hyun Song, Sun Young Joo, Se Jin Kim, Seung Hyun Jang, Ho Lee, Je Kyung Seong, Jae Young Choi, Heon Yung Gee and Jinsei Jung
Cells 2023, 12(18), 2328; https://doi.org/10.3390/cells12182328 - 21 Sep 2023
Cited by 2 | Viewed by 1568
Abstract
Genetic hearing loss is the most common hereditary sensorial disorder. Though more than 120 genes associated with deafness have been identified, unveiled causative genes and variants of diverse types of hearing loss remain. Herein, we identified a novel nonsense homozygous variant in CEP250 [...] Read more.
Genetic hearing loss is the most common hereditary sensorial disorder. Though more than 120 genes associated with deafness have been identified, unveiled causative genes and variants of diverse types of hearing loss remain. Herein, we identified a novel nonsense homozygous variant in CEP250 (c.3511C>T; p.Gln1171Ter) among the family members with progressive moderate sensorineural hearing loss in nonsyndromic autosomal recessive type but without retinal degeneration. CEP250 encodes C-Nap1 protein belonging to the CEP protein family, comprising 30 proteins that play roles in centrosome aggregation and cell cycle progression. The nonsense variant in CEP250 led to the early truncating protein of C-Nap1, which hindered centrosome localization; heterologous expression of CEP250 (c.3511C>T) in NIH3T3 cells within cilia expression condition revealed that the truncating C-Nap1 (p.Gln1171Ter) was not localized at the centrosome but was dispersed in the cytosol. In the murine adult cochlea, Cep250 was expressed in the inner and outer hair cells. Knockout mice of Cep250 showed significant hair cell degeneration and progressive hearing loss in auditory brainstem response. In conclusion, a nonsense variant in CEP250 results in a deficit of centrosome localization and hair cell degeneration in the cochlea, which is associated with the progression of hearing loss in humans and mice. Full article
(This article belongs to the Special Issue Cell Death in Health and Disease)
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13 pages, 1884 KiB  
Article
Macromolecule Translocation across the Intestinal Mucosa of HIV-Infected Patients by Transcytosis and through Apoptotic Leaks
by Susanne M. Krug, Carolin Grünhagen, Kristina Allers, Christian Bojarski, Joachim Seybold, Thomas Schneider, Jörg-Dieter Schulzke and Hans-Jörg Epple
Cells 2023, 12(14), 1887; https://doi.org/10.3390/cells12141887 - 18 Jul 2023
Viewed by 1200
Abstract
Based on indirect evidence, increased mucosal translocation of gut-derived microbial macromolecules has been proposed as an important pathomechanism in HIV infection. Here, we quantified macromolecule translocation across intestinal mucosa from treatment-naive HIV-infected patients, HIV-infected patients treated by combination antiretroviral therapy, and HIV-negative controls [...] Read more.
Based on indirect evidence, increased mucosal translocation of gut-derived microbial macromolecules has been proposed as an important pathomechanism in HIV infection. Here, we quantified macromolecule translocation across intestinal mucosa from treatment-naive HIV-infected patients, HIV-infected patients treated by combination antiretroviral therapy, and HIV-negative controls and analyzed the translocation pathways involved. Macromolecule permeability was quantified by FITC-Dextran 4000 (FD4) and horseradish peroxidase (HRP) flux measurements. Translocation pathways were addressed using cold inhibition experiments. Tight junction proteins were characterized by immunoblotting. Epithelial apoptosis was quantified and translocation pathways were further characterized by flux studies in T84 cell monolayers using inducers and inhibitors of apoptosis and endocytosis. In duodenal mucosa of untreated but not treated HIV-infected patients, FD4 and HRP permeabilities were more than a 4-fold increase compared to the HIV-negative controls. Duodenal macromolecule permeability was partially temperature-dependent and associated with epithelial apoptosis without altered expression of the analyzed tight junction proteins. In T84 monolayers, apoptosis induction increased, and both apoptosis and endocytosis inhibitors reduced macromolecule permeability. Using quantitative analysis, we demonstrate the increased macromolecule permeability of the intestinal mucosa in untreated HIV-infected patients. Combining structural and mechanistic studies, we identified two pathways of increased macromolecule translocation in HIV infection: transcytosis and passage through apoptotic leaks. Full article
(This article belongs to the Special Issue Cell Death in Health and Disease)
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Review

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27 pages, 3764 KiB  
Review
Unveiling the Neural Environment in Cancer: Exploring the Role of Neural Circuit Players and Potential Therapeutic Strategies
by Tuan Minh Nguyen, Dinh Thi Minh Ngoc, Jung-Hye Choi and Chang-Hoon Lee
Cells 2023, 12(15), 1996; https://doi.org/10.3390/cells12151996 - 3 Aug 2023
Cited by 7 | Viewed by 2899
Abstract
The regulation of the immune environment within the tumor microenvironment has provided new opportunities for cancer treatment. However, an important microenvironment surrounding cancer that is often overlooked despite its significance in cancer progression is the neural environment surrounding the tumor. The release of [...] Read more.
The regulation of the immune environment within the tumor microenvironment has provided new opportunities for cancer treatment. However, an important microenvironment surrounding cancer that is often overlooked despite its significance in cancer progression is the neural environment surrounding the tumor. The release of neurotrophic factors from cancer cells is implicated in cancer growth and metastasis by facilitating the infiltration of nerve cells into the tumor microenvironment. This nerve–tumor interplay can elicit cancer cell proliferation, migration, and invasion in response to neurotransmitters. Moreover, it is possible that cancer cells could establish a network resembling that of neurons, allowing them to communicate with one another through neurotransmitters. The expression levels of players in the neural circuits of cancers could serve as potential biomarkers for cancer aggressiveness. Notably, the upregulation of certain players in the neural circuit has been linked to poor prognosis in specific cancer types such as breast cancer, pancreatic cancer, basal cell carcinoma, and stomach cancer. Targeting these players with inhibitors holds great potential for reducing the morbidity and mortality of these carcinomas. However, the efficacy of anti-neurogenic agents in cancer therapy remains underexplored, and further research is necessary to evaluate their effectiveness as a novel approach for cancer treatment. This review summarizes the current knowledge on the role of players in the neural circuits of cancers and the potential of anti-neurogenic agents for cancer therapy. Full article
(This article belongs to the Special Issue Cell Death in Health and Disease)
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19 pages, 422 KiB  
Review
Pericyte Loss in Diseases
by Pengfei Li and Hongkuan Fan
Cells 2023, 12(15), 1931; https://doi.org/10.3390/cells12151931 - 26 Jul 2023
Cited by 15 | Viewed by 3567
Abstract
Pericytes are specialized cells located in close proximity to endothelial cells within the microvasculature. They play a crucial role in regulating blood flow, stabilizing vessel walls, and maintaining the integrity of the blood–brain barrier. The loss of pericytes has been associated with the [...] Read more.
Pericytes are specialized cells located in close proximity to endothelial cells within the microvasculature. They play a crucial role in regulating blood flow, stabilizing vessel walls, and maintaining the integrity of the blood–brain barrier. The loss of pericytes has been associated with the development and progression of various diseases, such as diabetes, Alzheimer’s disease, sepsis, stroke, and traumatic brain injury. This review examines the detection of pericyte loss in different diseases, explores the methods employed to assess pericyte coverage, and elucidates the potential mechanisms contributing to pericyte loss in these pathological conditions. Additionally, current therapeutic strategies targeting pericytes are discussed, along with potential future interventions aimed at preserving pericyte function and promoting disease mitigation. Full article
(This article belongs to the Special Issue Cell Death in Health and Disease)
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18 pages, 6265 KiB  
Review
Cracking the Code of Neuronal Cell Fate
by Giovanna Morello, Valentina La Cognata, Maria Guarnaccia, Velia D’Agata and Sebastiano Cavallaro
Cells 2023, 12(7), 1057; https://doi.org/10.3390/cells12071057 - 30 Mar 2023
Viewed by 1953
Abstract
Transcriptional regulation is fundamental to most biological processes and reverse-engineering programs can be used to decipher the underlying programs. In this review, we describe how genomics is offering a systems biology-based perspective of the intricate and temporally coordinated transcriptional programs that control neuronal [...] Read more.
Transcriptional regulation is fundamental to most biological processes and reverse-engineering programs can be used to decipher the underlying programs. In this review, we describe how genomics is offering a systems biology-based perspective of the intricate and temporally coordinated transcriptional programs that control neuronal apoptosis and survival. In addition to providing a new standpoint in human pathology focused on the regulatory program, cracking the code of neuronal cell fate may offer innovative therapeutic approaches focused on downstream targets and regulatory networks. Similar to computers, where faults often arise from a software bug, neuronal fate may critically depend on its transcription program. Thus, cracking the code of neuronal life or death may help finding a patch for neurodegeneration and cancer. Full article
(This article belongs to the Special Issue Cell Death in Health and Disease)
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