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Pharmacological Modulation of NLRP3: From Therapy Personalization to Innovative Drugs
Giulia Zudeh1, Sara Sossai2, Jacopo Angelini3
1Department of Translational and Advanced Diagnostics, Institute for Maternal and Child Health I.R.C.C.S. Burlo Garofolo, 34137 Trieste, Italy.
Frontiers in Bioscience (Landmark Edition)
|November 6, 2025
Summary
The nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome is crucial for inflammation. NLRP3 promoter methylation may predict glucocorticoid therapy response in inflammatory diseases.
Area of Science:
- Immunology
- Molecular Biology
- Pharmacology
Background:
- The NLRP3 inflammasome is a key regulator of innate immunity and pro-inflammatory cytokine secretion.
- Dysregulation of NLRP3 is linked to various diseases, including inflammatory bowel disease, arthritis, cancer, Alzheimer's disease, and type 2 diabetes.
- NLRP3 also plays a role in drug-related adverse reactions, making its modulation a potential therapeutic strategy.
Purpose of the Study:
- To review the pharmacological modulation of NLRP3 for regulating inflammatory processes and mitigating adverse drug reactions.
- To explore the role of post-transcriptional modifications, epigenetic factors (lncRNAs, DNA methylation), and interacting regulators in NLRP3 inflammasome activation.
- To highlight NLRP3 levels and promoter methylation as potential biomarkers for predicting drug response, specifically glucocorticoid therapy.
Main Methods:
- Literature review of compounds modulating NLRP3 activity.
- Analysis of studies investigating NLRP3 regulation by epigenetic factors.
- Examination of research linking NLRP3 expression and methylation to drug response.
Main Results:
- Pharmacological compounds can effectively modulate NLRP3, offering strategies for managing inflammatory conditions and drug side effects.
- NLRP3 inflammasome activation is influenced by epigenetic mechanisms, including long non-coding RNAs and DNA methylation.
- NLRP3 promoter methylation is emerging as a promising pharmacoepigenetic biomarker for predicting glucocorticoid therapy response in inflammatory diseases.
Conclusions:
- NLRP3 inflammasome is a critical target for therapeutic intervention in inflammatory diseases and adverse drug reactions.
- Epigenetic modifications, particularly NLRP3 promoter methylation, are significant regulators of NLRP3 inflammasome expression and function.
- NLRP3 promoter methylation represents a novel biomarker for personalized medicine, guiding glucocorticoid therapy selection in patients with inflammatory conditions.
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