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The Interplay Between Cellular Stress and Human Diseases
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The Interplay Between Cellular Stress and Human Diseases

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

Deadline for manuscript submissions: 20 February 2026 | Viewed by 2903

Special Issue Editor

Dr. Daniele Vergara

E-Mail Website
Guest Editor
Department of Biological and Environmental Sciences and Technologies, University of Salento, 73100 Lecce, Italy
Interests: cellular physiology; proteomics; cell plasticity; epithelial to mesenchymal transition; signal transduction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mammalian cells are subjected to a variety of stress conditions that significantly influence cellular responses. These adaptive mechanisms ensure the maintenance of cellular and systemic homeostasis. Overall, cellular stress response has a physiological and patho- physiological significance. The loss of these control mechanisms can lead to cellular senescence or regulated cell death, or trigger the onset of several human pathologies including cancer and neurodegenerative diseases. In cancer, these stress response mechanisms can increase tumor growth and progression. Therefore, strategies aimed at modulating these pathways have a potential clinical implications.

In this special issue, we welcomes reviews and original articles in the cellular stress response field. Potential topics include, but are not limited to: biological pathways and molecular mechanisms activated after a cellular stress response; the clinical impact of stress response mechanisms; acute or chronic perturbations that activate stress responses; stress factors that are responsible for changes in the transcriptome or the proteome; mechanisms of cell death; mechanisms of cell adaptation; stress signaling pathways and stress signaling markers.

Dr. Daniele Vergara
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

  • cellular stress
  • DNA damage response
  • unfolded protein response
  • autophagy
  • senescence
  • apoptosis
  • repair pathways
  • mitochondrial stress
  • nutrient deprivation
  • oxidative stress

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Published Papers (3 papers)

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Research

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24 pages, 12021 KB  
Article
Therapeutic Potential of Edaravone for Neuroprotection Following Global Cerebral Hypoxia
by Johanna Franziska Busse, Jonas Frai, Luca Ines Hamacher, Veronika Matschke, Carsten Theiss, Thomas Weber, Jennifer Herzog-Niescery and Sarah Stahlke
Int. J. Mol. Sci. 2025, 26(18), 9019; https://doi.org/10.3390/ijms26189019 - 16 Sep 2025
Viewed by 344
Abstract
Global cerebral hypoxia triggers (mal-)adaptive responses that can lead to neuronal damage. This study evaluated edaravone’s neuroprotective effects in a rat hypoxia model, focusing on sex differences, treatment durations, and behavioral outcomes. Male and female rats underwent global cerebral hypoxia induced by rocuronium, [...] Read more.
Global cerebral hypoxia triggers (mal-)adaptive responses that can lead to neuronal damage. This study evaluated edaravone’s neuroprotective effects in a rat hypoxia model, focusing on sex differences, treatment durations, and behavioral outcomes. Male and female rats underwent global cerebral hypoxia induced by rocuronium, with post-hypoxia edaravone treatment. Motor coordination and activity were assessed through exploratory behavior tests. Histological analyses evaluated neuronal integrity and apoptosis, while microglial activity and gene expression were analyzed via immunofluorescence and qPCR. Edaravone showed transient neuroprotective effects on motor behavior and early immune responses, particularly in the cerebellum and hippocampus. No gross morphological damage was observed, though functional impairments occurred despite preserved cytoarchitecture. Microglial activity was initially suppressed in treated and later activated in untreated hypoxic brains, suggesting modulating immune responses. Gene expression analysis revealed region-specific, time-dependent, and sex-specific changes, including early upregulation of CCR7, S100B, and NSE in treated animals. Males were more susceptible to hypoxic damage, while females showed higher baseline resistance and better functional recovery. Seven-day edaravone treatment increased apoptotic markers in male cerebellum, indicating sex-specific differences in cell death mechanisms. These findings highlight the potential for personalized therapy and underscore the importance of considering sex differences in both research and clinical practice. Full article
(This article belongs to the Special Issue The Interplay Between Cellular Stress and Human Diseases)
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Review

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27 pages, 1207 KB  
Review
Glial Cytokine and Metabolic Networks in Progressive Multiple Sclerosis: From Pathophysiology to Biomarkers and Therapeutic Strategies
by Henry Leonard Hohm, Rasmus Schuster, Victor Bogdan Buciu, Denis-Mihai Serban, Sebastian Ciurescu, Amalia Cornea, Abhinav Sharma, Daciana Nistor and Nilima Rajpal Kundnani
Int. J. Mol. Sci. 2025, 26(18), 8817; https://doi.org/10.3390/ijms26188817 - 10 Sep 2025
Viewed by 299
Abstract
Progressive multiple sclerosis (PMS) represents a distinct clinical and biological entity characterized by compartmentalized neuroinflammation, chronic glial activation, and resistance to conventional immunotherapies. Unlike relapsing MS, PMS is sustained by resident CNS immune networks, where activated microglia and astrocytes orchestrate persistent cytokine signaling—particularly [...] Read more.
Progressive multiple sclerosis (PMS) represents a distinct clinical and biological entity characterized by compartmentalized neuroinflammation, chronic glial activation, and resistance to conventional immunotherapies. Unlike relapsing MS, PMS is sustained by resident CNS immune networks, where activated microglia and astrocytes orchestrate persistent cytokine signaling—particularly involving TNF-α, IL-1β, and IL-6—through self-amplifying feedback loops. In this narrative review, we explore how these cytokines interact with oxidative stress, iron accumulation, mitochondrial dysfunction, and impaired autophagy to drive neurodegeneration. Human-based evidence is integrated with insights from experimental models to clarify translational mechanisms. We also highlight fluid biomarkers (e.g., GFAP, NfL) and imaging modalities (e.g., TSPO-PET, QSM) that reflect glial activity and disease progression in vivo. Age, sex hormones, and immunosenescence are discussed as modulators of cytokine expression. Finally, we review emerging therapeutic strategies that target glial metabolism and cytokine networks rather than peripheral immune cells, offering a systems-based framework for future PMS interventions and personalized disease monitoring. Full article
(This article belongs to the Special Issue The Interplay Between Cellular Stress and Human Diseases)
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20 pages, 1846 KB  
Review
Insight into the Regulation of NDRG1 Expression
by Concetta Saponaro, Nicola Gammaldi, Viviana Cavallo, Maria Antonieta Ramírez-Morales, Francesco Alfredo Zito, Margherita Sonnessa, Francesco Vari, Ilaria Serra, Simona De Summa, Anna Maria Giudetti, Marco Trerotola and Daniele Vergara
Int. J. Mol. Sci. 2025, 26(8), 3582; https://doi.org/10.3390/ijms26083582 - 10 Apr 2025
Cited by 2 | Viewed by 1629
Abstract
The N-Myc Downstream Regulated Gene 1 (NDRG1) protein, a member of a family of four, has emerged as a key regulator of various physiological and pathological processes. Extensive knowledge has been gained on the modulation of NDRG1 expression during endoplasmic reticulum stress, autophagy, [...] Read more.
The N-Myc Downstream Regulated Gene 1 (NDRG1) protein, a member of a family of four, has emerged as a key regulator of various physiological and pathological processes. Extensive knowledge has been gained on the modulation of NDRG1 expression during endoplasmic reticulum stress, autophagy, and hypoxia. Moreover, new functions have emerged in recent years. Notably, NDRG1 regulates cell differentiation, metabolism, autophagy and vesicular transport. This has raised interest in the molecular mechanisms that control the cellular levels and activity of NDRG1. A series of studies have shown that NDRG1 can be finely regulated at the transcriptional, post-transcriptional, and translational levels. In addition, processes that mediate protein degradation and clearance also play key roles. Furthermore, three different NDRG1 proteoforms with distinct functions have been identified. An important question is the extent to which these proteoforms contribute to the regulation of cellular functions. Given the growing clinical interest in NDRG1, this review provides an overview of the regulatory mechanisms that control NDRG1 abundance, helping to deepen our understanding of the complex mechanisms underlying protein regulation. Full article
(This article belongs to the Special Issue The Interplay Between Cellular Stress and Human Diseases)
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