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Cell Death in Human Diseases: Mechanisms, Biomarkers and Therapeutic Opportunities

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: 20 May 2026 | Viewed by 1656

Special Issue Editor


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Guest Editor
Houston Methodist Research Institute, 6670 Bertner Ave., Houston, TX 77030, USA
Interests: apoptosis; atherosclerosis; ER stress; molecular biology

Special Issue Information

Dear Colleagues,

Cell death is a fundamental biological process that shapes development, tissue homeostasis, immunity, and disease progression. In recent years, the discovery of novel regulated cell death modalities—including ferroptosis, pyroptosis, necroptosis, and immunogenic cell death—has revolutionized our understanding of the pathogenesis in cancer, neurodegeneration, metabolic disorders, cardiovascular disease, and autoimmunity.

This Special Issue aims to highlight advances in the molecular mechanisms, biomarkers, and translational aspects of regulated cell death. By bringing together original research articles and comprehensive reviews, the Special Issue will provide a platform to bridge basic science with clinical applications, offering insights into therapeutic strategies that modulate cell death for disease intervention.

This Special Issue welcomes original research articles, reviews, and translational studies highlighting both mechanistic insights and clinical relevance. The goal is to provide a comprehensive platform for integrating discoveries from molecular biology, pharmacology, and clinical medicine. Submissions may include, but are not limited to, the following:

  1. Molecular Pathways of Regulated Cell Death
    • Apoptosis, necroptosis, pyroptosis, ferroptosis, and beyond.
    • Cross-talk between cell death and survival signaling.
  2. Cell Death and Human Diseases
    • Cancer, neurodegenerative disorders, and cardiovascular and metabolic diseases.
    • Autoimmune and inflammatory conditions.
  3. Immunogenic Cell Death and Immunity
    • The role of cell death in shaping immune surveillance.
    • Implications for immunotherapy and vaccine development.
  4. Biomarkers and Detection Methods
    • Circulating and tissue biomarkers of cell death.
    • Imaging and omics-based approaches.
  5. Therapeutic Targeting of Cell Death
    • Small molecules, biologics, and nanomedicine.
    • Strategies for selective induction or inhibition of cell death.
  6. Cell Death in Regeneration and Tissue Engineering
    • Balancing cell death and survival in tissue repair.
    • Implications for stem cell therapy and organ regeneration.
  7. Emerging Frontiers
    • Novel forms of regulated cell death.
    • Computational and systems biology approaches.
We look forward to your contributions to this timely and impactful Special Issue.

Dr. Decha Pinkaew
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 250 words) can be sent to the Editorial Office for assessment.

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

  • cell death
  • apoptosis
  • necroptosis
  • ferroptosis
  • pyroptosis
  • human disease
  • biomarkers

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Published Papers (1 paper)

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Review

37 pages, 3226 KB  
Review
Crosstalk Between Autophagy and Paraptosis: A New Frontier in Cancer Therapy
by Sweata Hanson, Deiviga Murugan, Palli V. Jinsha, Anupama Binoy, Bipin G. Nair and Nandita Mishra
Int. J. Mol. Sci. 2026, 27(5), 2234; https://doi.org/10.3390/ijms27052234 - 27 Feb 2026
Viewed by 900
Abstract
Autophagy and paraptosis are two distinct physiological mechanisms involved in regulating cell fate in cancer. Recent studies have demonstrated that autophagy is a crucial process for maintaining cellular homeostasis by facilitating the removal of misfolded proteins and damaged organelles. However, autophagy is found [...] Read more.
Autophagy and paraptosis are two distinct physiological mechanisms involved in regulating cell fate in cancer. Recent studies have demonstrated that autophagy is a crucial process for maintaining cellular homeostasis by facilitating the removal of misfolded proteins and damaged organelles. However, autophagy is found to play a dual role in cancer. Severe ER and mitochondrial dysfunction can trigger different forms of programmed cell death, including autophagic cell death. In cancer cells that evade apoptosis, paraptosis, a caspase-independent alternate death pathway, is triggered by ER and mitochondrial swelling, leading to extensive cytoplasmic vacuolation. It can be induced by natural compounds, metallic complexes, nanoparticles, or chemotherapeutic agents, primarily through excessive ROS production and disruption of protein, thiol, and calcium/ion homeostasis. Autophagy and paraptosis have been found to be connected through crosstalk. While MAPK activation drives paraptosis, ER stress and the unfolded protein response (UPR) can initiate both paraptosis and autophagy. UPR-mediated PERK activation promotes survival autophagy in ER-stressed melanoma, whereas PERK elimination triggers paraptosis via sec61β with unresolved ER stress. Similarly, CHOP and DDIT4 can enhance ER stress and proteotoxicity, thereby favouring paraptosis. This review is unique in exploring the dynamic interplay between autophagy and paraptosis in cancer cells, highlighting promising therapeutic targets for chemotherapy-resistant cancers. Full article
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