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Cells
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Factsheets of Cell Death
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Factsheets of Cell Death

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (5 October 2022) | Viewed by 13945

Special Issue Editor

Dr. Frank Eßmann

E-Mail Website
Guest Editor
Department of Molecular Medicine, Interfaculty Institute for Biochemistry, University of Tübingen, 72076 Tübingen, Germany
Interests: mutation; cancer; DNA damage

Special Issue Information

Dear Colleagues,

Cell death mechanisms and their corruption are central to development, tissue homeostasis, oncogenesis, and anti-cancer therapy. The principle mechanisms underlying the regulation of cell death have reached textbook status; death receptor signaling, mitochondrial apoptosis, caspase activation, apoptosis inhibitors, and BCL-2 protein family function have been studied in great detail. Nevertheless, new molecular clues and peculiarities are constantly being uncovered that offer sophisticated opportunities for therapeutic intervention in tumors. Perfect examples are specific small molecule inhibitors that block the activity of anti-apoptotic proteins.

This special issue´s aim is to sum up the current state of knowledge on cell death regulation and spice it up with exemplary data or latest findings.

Dr. Frank Eßmann
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. 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

  • apoptosis
  • necroptosis
  • ferroptosis
  • autophagy
  • death receptor
  • death inducing signaling complex
  • DISC
  • mitochondria
  • apoptosome
  • caspase
  • IAP
  • BCL-2 family
  • anti-apoptotic
  • pro-apoptotic
  • BH3-only
  • BH3-mimetic

Published Papers (3 papers)

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Research

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25 pages, 7901 KiB  
Article
The E3 Ligase TRIM25 Impairs Apoptotic Cell Death in Colon Carcinoma Cells via Destabilization of Caspase-7 mRNA: A Possible Role of hnRNPH1
by Usman Nasrullah, Kristina Stanke, Victoria Recknagel, Süleyman Bozkurt, Patrick Wurzel, Stefan Gauer, Gergely Imre, Christian Münch, Josef Pfeilschifter and Wolfgang Eberhardt
Cells 2023, 12(1), 201; https://doi.org/10.3390/cells12010201 - 03 Jan 2023
Cited by 1 | Viewed by 4838
Abstract
Therapy resistance is still a major reason for treatment failure in colorectal cancer (CRC). Previously, we identified the E3 ubiquitin ligase TRIM25 as a novel suppressor of caspase-2 translation which contributes to the apoptosis resistance of CRC cells towards chemotherapeutic drugs. Here, we [...] Read more.
Therapy resistance is still a major reason for treatment failure in colorectal cancer (CRC). Previously, we identified the E3 ubiquitin ligase TRIM25 as a novel suppressor of caspase-2 translation which contributes to the apoptosis resistance of CRC cells towards chemotherapeutic drugs. Here, we report the executioner caspase-7 as being a further target of TRIM25. The results from the gain- and loss-of-function approaches and the actinomycin D experiments indicate that TRIM25 attenuates caspase-7 expression mainly through a decrease in mRNA stability. The data from the RNA pulldown assays with immunoprecipitated TRIM25 truncations indicate a direct TRIM25 binding to caspase-7 mRNA, which is mediated by the PRY/SPRY domain, which is also known to be highly relevant for protein–protein interactions. By employing TRIM25 immunoprecipitation, we identified the heterogeneous nuclear ribonucleoprotein H1 (hnRNPH1) as a novel TRIM25 binding protein with a functional impact on caspase-7 mRNA stability. Notably, the interaction of both proteins was highly sensitive to RNase A treatment and again depended on the PRY/SPRY domain, thus indicating an indirect interaction of both proteins which is achieved through a common RNA binding. Ubiquitin affinity chromatography showed that both proteins are targets of ubiquitin modification. Functionally, the ectopic expression of caspase-7 in CRC cells caused an increase in poly ADP-ribose polymerase (PARP) cleavage concomitant with a significant increase in apoptosis. Collectively, the negative regulation of caspase-7 by TRIM25, which is possibly executed by hnRNPH1, implies a novel survival mechanism underlying the chemotherapeutic drug resistance of CRC cells. The targeting of TRIM25 could therefore offer a promising strategy for the reduction in therapy resistance in CRC patients. Full article
(This article belongs to the Special Issue Factsheets of Cell Death)
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Review

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14 pages, 1209 KiB  
Review
Pyroptosis and Its Role in SARS-CoV-2 Infection
by Zsofia Agnes Bittner, Markus Schrader, Shilpa Elizabeth George and Ralf Amann
Cells 2022, 11(10), 1717; https://doi.org/10.3390/cells11101717 - 23 May 2022
Cited by 16 | Viewed by 4213
Abstract
The pore-forming inflammatory cell death pathway, pyroptosis, was first described in the early 1990s and its role in health and disease has been intensively studied since. The effector molecule GSDMD is cleaved by activated caspases, mainly Caspase 1 or 11 (Caspase 4/5 in [...] Read more.
The pore-forming inflammatory cell death pathway, pyroptosis, was first described in the early 1990s and its role in health and disease has been intensively studied since. The effector molecule GSDMD is cleaved by activated caspases, mainly Caspase 1 or 11 (Caspase 4/5 in humans), downstream of inflammasome formation. In this review, we describe the molecular events related to GSDMD-mediated pore formation. Furthermore, we summarize the so far elucidated ways of SARS-CoV-2 induced NLRP3 inflammasome formation leading to pyroptosis, which strongly contributes to COVID-19 pathology. We also explore the potential of NLRP3 and GSDMD inhibitors as therapeutics to counter excessive inflammation. Full article
(This article belongs to the Special Issue Factsheets of Cell Death)
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13 pages, 1392 KiB  
Review
Eryptosis: Programmed Death of Nucleus-Free, Iron-Filled Blood Cells
by Peter Dreischer, Michael Duszenko, Jasmin Stein and Thomas Wieder
Cells 2022, 11(3), 503; https://doi.org/10.3390/cells11030503 - 01 Feb 2022
Cited by 31 | Viewed by 4004
Abstract
Human erythrocytes are organelle-free cells packaged with iron-containing hemoglobin, specializing in the transport of oxygen. With a total number of approximately 25 trillion cells per individual, the erythrocyte is the most abundant cell type not only in blood but in the whole organism. [...] Read more.
Human erythrocytes are organelle-free cells packaged with iron-containing hemoglobin, specializing in the transport of oxygen. With a total number of approximately 25 trillion cells per individual, the erythrocyte is the most abundant cell type not only in blood but in the whole organism. Despite their low complexity and their inability to transcriptionally upregulate antioxidant defense mechanisms, they display a relatively long life time, of 120 days. This ensures the maintenance of tissue homeostasis where the clearance of old or damaged erythrocytes is kept in balance with erythropoiesis. Whereas the regulatory mechanisms of erythropoiesis have been elucidated over decades of intensive research, the understanding of the mechanisms of erythrocyte clearance still requires some refinement. Here, we present the main pathways leading to eryptosis, the programmed death of erythrocytes, with special emphasis on Ca2+ influx, the generation of ceramide, oxidative stress, kinase activation, and iron metabolism. We also compare stress-induced erythrocyte death with erythrocyte ageing and clearance, and discuss the similarities between eryptosis and ferroptosis, the iron-dependent regulated death of nucleated blood cells. Finally, we focus on the pathologic consequences of deranged eryptosis, and discuss eryptosis in the context of different infectious diseases, e.g., viral or parasitic infections, and hematologic disorders. Full article
(This article belongs to the Special Issue Factsheets of Cell Death)
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