SynthesisCell communication and signaling : CCS2025
The impact of post-translational modifications and subcellular localization on NLRP3 inflammasome activation: A systematic review.
Synthesis in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- The Role of Skeletal Muscle Mitochondria in NLRP3 Inflammasome Signaling.Biomolecules · 2026Review
- TRIM21 facilitates inflammasome assembly and contributes to autoinflammatory disease.Nature communications · 2026Article
- Gene Expression Profiles in the Optic Nerve of Mice with Systemic Acanthamoebiasis.International journal of molecular sciences · 2026Article
- NLRP3 inflammasome in acute kidney injury: molecular mechanisms, post-translational regulation, and immunotherapeutic potential.Frontiers in immunology · 2026Review
- The interplay between NLRP3 inflammasome and metabolic signals in gouty arthritis.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundThe NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome is crucial for innate immunity. However, its uncontrolled and dysregulated activation may cause various inflammatory and autoimmune disorders. Therefore, tight regulation of NLRP3 inflammasome is necessary. Numerous post-translational modifications (PTMs) are reported to play a critical role in regulating NLRP3 inflammasome activation, including (de-)phosphorylation, (de-)ubiquitination, (de-)SUMOylation, (de-)palmitoylation, (de-)acetylation, deglutathionylation, ISGylation, S-nitrosylation, and alkylation. In addition, the subcellular localization of NLRP3, involving endoplasmic reticulum (ER), mitochondria, Golgi, endosomes, and the microtubule-organizing center (MTOC), is also closely related to inflammasome assembly and activation. AIMS OF REVIEW: This review first describes the effects of recently found PTMs on NLRP3 inflammasome activation. Furthermore, the stage at which PTMs occur is elucidated in detail while previous reviews do not distinguish it very clearly. In addition, based on the subcellular distribution of NLRP3, this review proposes a novel spatiotemporal activation of this inflammasome. KEY SCIENTIFIC CONCEPTS OF REVIEW: This review highlights the innovative findings about the effects of PTMs and localization on NLRP3 inflammasome, which enrich the regulatory networks of this inflammasome and offer references for potential clinical translation in the future.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.