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Cells
Special Issues
Cell Death: Cell–Cell Interactions and Signaling Networks
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Cell Death: Cell–Cell Interactions and Signaling Networks

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

Deadline for manuscript submissions: closed (31 March 2025) | Viewed by 2393

Special Issue Editors

Dr. Manas Ranjan Gartia

E-Mail Website
Guest Editor
Department of Mechanical and Industrial Engineering Louisiana State University , 3261 Patrick F. Taylor Hall, Baton Rouge, LA 70803, USA
Interests: spatial lipidomics; ferroptosis; Raman spectroscopy; cell death mechanism
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Sun Chul Kang

E-Mail Website
Guest Editor
Department of Biotechnology, College of Engineering, Daegu University, Gyeongsan 38453, Gyeongbook, Republic of Korea
Interests: cancer biology; drug resistance; nanomedicine; development of diagnostic kits; stem cell research; genotoxicity research
Dr. Sukkum Ngullie Chang

E-Mail Website
Guest Editor
Department of Mechanical & Industrial Engineering, Louisiana State University, Baton Rouge, LA 70803, USA
Interests: drug resistance; cancer biology; cell signaling; inflammation; fibrosis

Special Issue Information

Dear Colleagues,

Cell death is a crucial and fundamental biological process. The Nomenclature Committee on Cell Death (NCCD) has set guidelines to interpret cell death from morphological, biochemical, and functional viewpoints, enabling the identification of various distinct types of cell death, each defined by specific mechanisms and biological implications. Interactions between cells during this process play a critical role in maintaining tissue homeostasis, coordinating immune responses, and modulating the local microenvironment. These interactions may involve various signaling molecules, receptors, and physical contacts, and can vary depending on the type of cell death involved.

We welcome submissions of studies investigating cell-to-cell interactions and the complex molecular mechanisms triggering cell death response. This encompasses research on intrinsic and extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entosis, NETosis, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, mitotic catastrophe, and other emerging cell death events and mechanisms. We encourage studies to be submitted that are conducted on humans, mice, cell lines, and other model systems.

Dr. Manas Ranjan Gartia
Prof. Dr. Sun Chul Kang
Dr. Sukkum Ngullie Chang
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

  • apoptosis
  • necrosis
  • pyroptosis
  • autophagic cell death
  • lysosome-dependent cell death
  • parthanatos
  • ferroptosis
  • anoikis
  • entosis
  • necroptosis
  • NETosis
  • mitotic catastrophe
  • healthy cell death tissue homeostasis

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Published Papers (2 papers)

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Research

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18 pages, 4083 KiB  
Article
The Assessment of the Effect of Autophagy Inhibitors—Chloroquine and 3-Methyladenine on the Antitumor Activity of Trametinib Against Amelanotic Melanoma Cells
by Dominika Stencel, Justyna Kowalska, Zuzanna Rzepka, Klaudia Banach, Marta Karkoszka-Stanowska and Dorota Wrześniok
Cells 2025, 14(7), 557; https://doi.org/10.3390/cells14070557 - 7 Apr 2025
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Abstract
Malignant melanoma, particularly amelanotic melanoma, contributes to a very serious problem in public health. One way to find new therapies is to learn about and understand the molecular pathways that regulate cancer growth and development. In the case of a tumor, the autophagy [...] Read more.
Malignant melanoma, particularly amelanotic melanoma, contributes to a very serious problem in public health. One way to find new therapies is to learn about and understand the molecular pathways that regulate cancer growth and development. In the case of a tumor, the autophagy process can lead to the development or inhibition of cancer. This study aimed to assess the cytotoxicity of connection trametinib (MEK1 and MEK2 kinase inhibitor) with autophagy inhibitors—chloroquine (lysosomal clearance of autophagosomes inhibitor) and 3-methyladenine (phosphatidylinositol 3-kinases inhibitor), on two amelanotic melanoma cell lines (C32 and A-375). The results showed that combination therapy had better anti-proliferative effects than alone therapy in both cell lines. The C32 cell line was more sensitive to 3-methyladenine treatment (alone and in combinations), and the A375 line showed sensitivity to chloroquine and 3-methyladenine (alone and in combinations). The anti-proliferative effect was accompanied by dysregulation of the cell cycle, a decrease in the reduced thiols, the depolarization of the mitochondrial membrane and the level of p44/p42 MAPK. Both inhibitors have the ability to induce apoptosis. Differences in the level of LC3A/B and LC3B proteins between the chloroquine and the 3-methyladenine samples indicate that these drugs inhibit autophagy at different stages. The enhancement of the effect of trametinib by autophagy inhibitors suggests the possibility of combining drugs with anti-cancer potential with modulators of the autophagy process. Full article
(This article belongs to the Special Issue Cell Death: Cell–Cell Interactions and Signaling Networks)
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Review

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19 pages, 1388 KiB  
Review
SASP Modulation for Cellular Rejuvenation and Tissue Homeostasis: Therapeutic Strategies and Molecular Insights
by Saud Alqahtani, Taha Alqahtani, Krishnaraju Venkatesan, Durgaramani Sivadasan, Rehab Ahmed, Nizar Sirag, Hassabelrasoul Elfadil, Hanem Abdullah Mohamed, Haseena T.A., Rasha Elsayed Ahmed, Pooja Muralidharan and Premalatha Paulsamy
Cells 2025, 14(8), 608; https://doi.org/10.3390/cells14080608 - 17 Apr 2025
Viewed by 1360
Abstract
Cellular senescence regulates aging, tissue maintenance, and disease progression through the Senescence-Associated Secretory Phenotype (SASP), a secretory profile of cytokines, chemokines, growth factors, and matrix-remodeling enzymes. While transient SASP aids wound healing, its chronic activation drives inflammation, fibrosis, and tumorigenesis. This review examines [...] Read more.
Cellular senescence regulates aging, tissue maintenance, and disease progression through the Senescence-Associated Secretory Phenotype (SASP), a secretory profile of cytokines, chemokines, growth factors, and matrix-remodeling enzymes. While transient SASP aids wound healing, its chronic activation drives inflammation, fibrosis, and tumorigenesis. This review examines SASP’s molecular regulation, dual roles in health and pathology, and therapeutic potential. The following two main strategies are explored: senescence clearance, which eliminates SASP-producing cells, and SASP modulation, which refines secretion to suppress inflammation while maintaining regenerative effects. Key pathways, including NF-κB, C/EBPβ, and cGAS-STING, are discussed alongside pharmacological, immunotherapeutic, gene-editing, and epigenetic interventions. SASP heterogeneity necessitates tissue-specific biomarkers for personalized therapies. Challenges include immune interactions, long-term safety, and ethical considerations. SASP modulation emerges as a promising strategy for aging, oncology, and tissue repair, with future advancements relying on multi-omics and AI-driven insights to optimize clinical outcomes. Full article
(This article belongs to the Special Issue Cell Death: Cell–Cell Interactions and Signaling Networks)
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