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Cell Fate Decisions: Autophagy, Apoptosis, Pyroptosis, Necroptosis, Ferroptosis and PANoptosis in Health and Disease

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 September 2025 | Viewed by 1005

Special Issue Editor

St. Jude Children's Research Hospital, Memphis, TN, USA
Interests: cell death; cellular signaling; innate immunity

Special Issue Information

Dear Colleagues,

The decisions that govern cellular life and death play a crucial role in maintaining homeostasis and shaping the pathological landscape of diseases. Genetic programs and regulatory networks driving cell survival and death are fundamental for understanding human biology and developing novel therapeutics. Recent advancements in regulated cell death pathways have highlighted the unique characteristics of distinct cell death modalities. While apoptotic cell death is largely non-immunogenic, forms like pyroptosis, necroptosis, and PANoptosis are predominantly pro-inflammatory. The immunomodulatory potential of ferroptosis is still being unraveled, offering exciting new avenues for research. Autophagy, traditionally viewed as a protective mechanism antagonizing several cell death pathways and inflammation, can also paradoxically promote cell death under certain conditions.

Given the intricate links between cell death and survival pathways, mutations in the genes regulating these processes often lead to developmental defects in animals and immune deficiencies or autoinflammatory diseases in humans. Thus, novel phenotypic observations and further mechanistic insights into this fundamental cellular decision network will be the key to innovative therapeutic strategies and a better understanding of health and disease.

In this Special Issue, “Cell Fate Decisions: Autophagy, Apoptosis, Pyroptosis, Necroptosis, Ferroptosis and PANoptosis in Health and Disease”, we invite original research articles and thought-provoking reviews that reveal novel phenotypes, explore the mechanisms initiating, mediating, executing, or antagonizing cell death in different cell types and across diverse pathophysiological settings. We aim to be conceptually inspiring and advance the field toward novel, interesting and impactful discoveries.

Dr. Yaqiu Wang
Guest Editor

Manuscript Submission Information

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Keywords

  • inflammation
  • autophagy
  • apoptosis
  • pyroptosis
  • necroptosis
  • PANoptosis
  • ferroptosis
  • cell death
  • cell survival

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Published Papers (1 paper)

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Research

11 pages, 4065 KiB  
Article
NSP6 of SARS-CoV-2 Dually Regulates Autophagic–Lysosomal Degradation
by Haijiao Zhang, Jianying Chang and Ren Sheng
Int. J. Mol. Sci. 2025, 26(8), 3699; https://doi.org/10.3390/ijms26083699 - 14 Apr 2025
Viewed by 265
Abstract
The pandemic of coronavirus disease 2019 (COVID-19), brought about by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has significantly impacted public health and the economy. A fundamental aspect of addressing this virus lies in elucidating the mechanisms through which it induces disease. [...] Read more.
The pandemic of coronavirus disease 2019 (COVID-19), brought about by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has significantly impacted public health and the economy. A fundamental aspect of addressing this virus lies in elucidating the mechanisms through which it induces disease. Our study reveals that Non-structural protein 6 (NSP6) of SARS-CoV-2 promotes the initiation of autophagy by activating Beclin1. In the later stage of autophagy, however, NSP6 causes a blockage in the autophagy–lysosome degradation via the inhibition of Mucolipin 1 (MLN1). The single nucleotide polymorphism (SNP) L37F in NSP6, which is associated with asymptomatic infection, similarly enhances the initiation of autophagy but displays a reduced ability to impede lysosome-dependent degradation. In summary, we demonstrated the dual-regulation mechanism of NSP6 in autophagy, which may be one of the reasons for targeting cellular autophagy to induce viral pathogenesis. This finding may provide promising new directions for future research and clinical interventions. Full article
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