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Cell Apoptosis, 3rd Edition
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Cell Apoptosis, 3rd Edition

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

Deadline for manuscript submissions: 30 November 2024 | Viewed by 2731

Special Issue Editor

Prof. Dr. Francisco Estevez

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Guest Editor
Department of Biochemistry and Molecular Biology, University Institute for Biomedical and Healthcare Research (IUIBS), University of Las Palmas de Gran Canaria, 35016 Las Palmas de Gran Canaria, Spain
Interests: apoptosis; caspase; cell cycle; cell proliferation; cytotoxicity; in vitro antiproliferative activity; mitogen-activated protein kinases; reactive oxygen species; structure–activity relationship
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Apoptosis is a form of regulated cell death that plays a major role in an array of physiological and pathophysiological conditions. The execution of apoptosis is triggered by distinct and interconnected signaling pathways. Together with sustained proliferative signaling, the resistance to apoptosis is recognized as one of the cellular hallmarks of cancer. Exponential progress in our understanding of the regulation of death and survival signaling cascades has recently been achieved. This includes the executioners of apoptosis, B-cell lymphoma 2 family proteins, and oxidative stress. New advances in this field will allow for the identification of new modulators of the pathways in cell death and survival. This knowledge may contribute to the preparation of therapeutic strategies of interest in medicine. It includes the ability to potentiate the cytotoxicity against malignant cells and has potential application in other metabolic or immunological diseases. This Special Issue aims to improve our understanding of the molecular mechanisms involved in apoptosis. Contributions may relate to the events triggered by different physical and chemical agents, including naturally occurring and synthetic compounds, and/or by physiological and pathophysiological conditions.

More published papers can be found in the closed Special Issue “Cell Apoptosis” and “Cell Apoptosis 2.0”.

Prof. Dr. Francisco Estevez
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

  • apoptosis
  • caspase
  • cell cycle
  • cytotoxicity
  • reactive oxygen species

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Published Papers (2 papers)

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18 pages, 4870 KiB  
Article
The Role of PD-1/PD-L1 and IL-7 in Lymphocyte Dynamics and Sepsis Progression: A Biomarker Study in Critically Ill Patients
by Oana Coman, Bianca-Liana Grigorescu, Adina Huțanu, Anca Bacârea, Anca Meda Văsieșiu, Raluca Ștefania Fodor, Marius Petrișor and Leonard Azamfirei
Int. J. Mol. Sci. 2024, 25(23), 12612; https://doi.org/10.3390/ijms252312612 (registering DOI) - 24 Nov 2024
Abstract
Sepsis pathophysiology involves a dysregulated immune response to infection, excessive inflammation, and immune paralysis. This study explores the relationships between cell death biomarkers (serum-soluble levels of programmed cell death protein 1 (PD-1), programmed death ligand 1 (PD-L1), and interleukin-7 (IL-7)) and the percentages [...] Read more.
Sepsis pathophysiology involves a dysregulated immune response to infection, excessive inflammation, and immune paralysis. This study explores the relationships between cell death biomarkers (serum-soluble levels of programmed cell death protein 1 (PD-1), programmed death ligand 1 (PD-L1), and interleukin-7 (IL-7)) and the percentages of various lymphocyte subsets in relation to the severity and progression of sepsis. This prospective, observational study included 87 critically ill patients. We monitored parameters on days 1 (sepsis was diagnosed according to the Sepsis-3 Consensus) and 5. We established an IL-7 cutoff value of 1.94 pg/mL by comparing levels between a healthy control group and patients with sepsis (p < 0.0001). Lymphopenia was observed in all patients, with negative correlations between helper T lymphocytes and cytotoxic and B lymphocytes, and positive correlations involving cytotoxic lymphocytes across all groups. We found correlations between PD-1/PD-L1 and lymphocyte subsets. IL-7 showed a statistical correlation with PD-1 in non-survivors. Assessing lymphocyte levels shows potential as a biomarker for evaluating the progression of sepsis. Monitoring IL-7 levels could help assess survival, as low levels are associated with higher mortality risk. Monitoring IL-7 levels could help assess survival, as low levels are associated with higher mortality risk. Elevated PD-1/PD-L1 expression impairs costimulatory signalling, reducing T cell responses and lymphopenia, which increases the risk of nosocomial infections. Full article
(This article belongs to the Special Issue Cell Apoptosis, 3rd Edition)
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Review

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43 pages, 4610 KiB  
Review
Significance of Programmed Cell Death Pathways in Neurodegenerative Diseases
by Dong Guo, Zhihao Liu, Jinglin Zhou, Chongrong Ke and Daliang Li
Int. J. Mol. Sci. 2024, 25(18), 9947; https://doi.org/10.3390/ijms25189947 - 15 Sep 2024
Cited by 1 | Viewed by 2261
Abstract
Programmed cell death (PCD) is a form of cell death distinct from accidental cell death (ACD) and is also referred to as regulated cell death (RCD). Typically, PCD signaling events are precisely regulated by various biomolecules in both spatial and temporal contexts to [...] Read more.
Programmed cell death (PCD) is a form of cell death distinct from accidental cell death (ACD) and is also referred to as regulated cell death (RCD). Typically, PCD signaling events are precisely regulated by various biomolecules in both spatial and temporal contexts to promote neuronal development, establish neural architecture, and shape the central nervous system (CNS), although the role of PCD extends beyond the CNS. Abnormalities in PCD signaling cascades contribute to the irreversible loss of neuronal cells and function, leading to the onset and progression of neurodegenerative diseases. In this review, we summarize the molecular processes and features of different modalities of PCD, including apoptosis, necroptosis, pyroptosis, ferroptosis, cuproptosis, and other novel forms of PCD, and their effects on the pathogenesis of neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), amyotrophic lateral sclerosis (ALS), spinal muscular atrophy (SMA), multiple sclerosis (MS), traumatic brain injury (TBI), and stroke. Additionally, we examine the key factors involved in these PCD signaling pathways and discuss the potential for their development as therapeutic targets and strategies. Therefore, therapeutic strategies targeting the inhibition or facilitation of PCD signaling pathways offer a promising approach for clinical applications in treating neurodegenerative diseases. Full article
(This article belongs to the Special Issue Cell Apoptosis, 3rd Edition)
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