Crosstalk between NLRP3 signaling and histone deacetylases in inflammasome-driven diseases
The NLRP3 inflammasome is a validated therapeutic target in inflammatory, metabolic, and neurodegenerative diseases. Epigenetic regulators, particularly histone deacetylases (HDACs), have emerged as key modulators of inflammasome priming and activation. Recent advances in medicinal chemistry have pr...
| Autores: | , , , , , , |
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| Tipo de recurso: | artículo |
| Fecha de publicación: | 2025 |
| País: | España |
| Institución: | Universidad Autónoma de Madrid |
| Repositorio: | Biblos-e Archivo. Repositorio Institucional de la UAM |
| Idioma: | inglés |
| OAI Identifier: | oai:repositorio.uam.es:10486/744320 |
| Acceso en línea: | https://hdl.handle.net/10486/744320 https://dx.doi.org/10.1021/acs.jmedchem.5c02657 |
| Access Level: | acceso embargado |
| Palabra clave: | Neurodegenerative diseases epigenetic regulators histone deacetylases inflammasomes Química |
| Sumario: | The NLRP3 inflammasome is a validated therapeutic target in inflammatory, metabolic, and neurodegenerative diseases. Epigenetic regulators, particularly histone deacetylases (HDACs), have emerged as key modulators of inflammasome priming and activation. Recent advances in medicinal chemistry have provided new chemical modalities for the mechanistic interrogation and the potential therapeutic modulation of NLRP3 signaling. This Perspective dissects the mechanistic interface between HDAC-dependent epigenetic control and NLRP3 signaling and highlights emerging chemical tools, including isoform-selective inhibitors and targeted protein degraders. We discuss the challenges of isoform selectivity, species-specific differences, and the therapeutic potential of HDAC-based strategies to attenuate aberrant NLRP3 activity while minimizing off-target effects. Understanding this epigenetic-inflammasome crosstalk may provide a framework for translating epigenetic modulation into innovative treatments for inflammasome-driven diseases |
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