New Insights into Inflammasome: Mechanisms of Activation, Cell Death, and Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 954

Special Issue Editor


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Guest Editor
Molecular Pathology and Pharmacogenetics Group, Instituto Murciano de Investigación Biosanitaria Pascual Parrilla–IMIB, Murcia, Spain
Interests: inflammasome; NLRP3; inflammation; immunology; innate immunity

Special Issue Information

Dear Colleagues,

Since the discovery of the first inflammasome in the early 2000s, our understanding of inflammasomes has profoundly advanced. These multiprotein complexes play a critical role in the innate immune response by detecting pathogenic microorganisms and endogenous stress signals. Upon activation, the inflammasomes initiate a cascade of events leading to the production of pro-inflammatory cytokines and a form of programmed cell death known as pyroptosis. This process is crucial for the elimination of infections and damaged cells and the restoration of homeostasis. However, dysregulated inflammasome activity has been strongly linked to numerous chronic inflammatory diseases, including neurodegenerative disorders, metabolic syndromes, and cancer. Moreover, gain-of-function mutations in the inflammasome sensors are responsible for various autoinflammatory syndromes. A deeper understanding of the activation and cell death mechanisms they trigger opens new avenues for therapeutic interventions to modulate inflammasome components to treat these diseases.

Therefore, in this Special Issue, we invite you to submit your articles to contribute to the latest advancements in inflammasome research, offering valuable insights for scientists and clinicians. Manuscripts providing translational value will be particularly welcome.

Dr. Ana Tapia-Abellán
Guest Editor

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Keywords

  • inflammasomes
  • inflammation
  • pyroptosis
  • chronic diseases
  • autoinflammatory syndromes

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Published Papers (1 paper)

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Review

39 pages, 2145 KiB  
Review
NLRP3 Inflammasome and Inflammatory Response in Aging Disorders: The Entanglement of Redox Modulation in Different Outcomes
by Bhavana Chhunchha, Eri Kubo, Deepali Lehri and Dhirendra P. Singh
Cells 2025, 14(13), 994; https://doi.org/10.3390/cells14130994 - 29 Jun 2025
Viewed by 788
Abstract
Increasing evidence reveals that the deregulation of cellular antioxidant response with advancing age, resulting in the continuing amplification of oxidative stress-induced inflammatory response, is a pre-eminent cause for the onset of aging-related disease states, including blinding diseases. However, several safeguards, like an antioxidant [...] Read more.
Increasing evidence reveals that the deregulation of cellular antioxidant response with advancing age, resulting in the continuing amplification of oxidative stress-induced inflammatory response, is a pre-eminent cause for the onset of aging-related disease states, including blinding diseases. However, several safeguards, like an antioxidant defense system, are genetically in place to maintain redox homeostasis. Nonetheless, if the homeostatic capacity of such systems fails (like in aging), an inflammatory pathway elicited by excessive oxidative stress-evoked aberrant NLRP3 (NOD, LRR- and pyrin domain-containing protein 3) inflammasome activation can become pathogenic and lead to disease states. Among all known inflammasomes, NLRP3 is the most studied and acts as an intracellular sensor to detect danger(s). Upon activation, NLRP3 recruits apoptosis-associated speck-like protein containing a CARD (ASC) oligomerization and facilitates the recruitment of activated Caspase-1 (Cas-1), which results in the release of inflammatory cytokines, IL-1β and IL-18 and the activation of GasderminD, an executor of pyroptosis. NLRP3 inflammasome is tightly regulated in favor of cell health. However, when and how the activation of NLRP3 and its inflammatory components goes awry, leading to cellular derangement, and what regulatory factors are involved in the normal physiological and aging/oxidative conditions will be included in this review. Also, we address the latest findings to highlight the connection between oxidative stress, antioxidants, and NLRP3 activation as this begets aging diseases and explore the cellular pathways that are in place to regulate oxidative-induced inflammations and the pathobiological consequences of dysregulated inflammatory responses and vice versa. Full article
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