ReviewNaunyn-Schmiedeberg's archives of pharmacology2025
NLRP3 inflammasome-based therapies by natural products: a new development in the context of cancer therapy.
Review in Naunyn-Schmiedeberg's archives of pharmacology, 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Mechanistic insights into natural product-driven modulation of NLRP3-inflammasome signalling in metabolic syndrome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Modulation of AMPK/SIRT1 signaling by piribedil attenuates cyclophosphamide-induced nephrotoxicity via PI3K/Akt, MAPKs, and TLR4/NLRP3 pathways with regulation of KIM-1/NGAL.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Soyeom-Jetong mixture attenuates NLRP3 inflammasome-mediated inflammation.Frontiers in pharmacology · 2026Article
- Coenzyme Q10 Ameliorates Chemotherapy-Induced Neurotoxicity in iPSC-Derived Neurons by Reducing Oxidative Stress.International journal of molecular sciences · 2025Article
- Leucine-rich repeat neuronal 1 as a prognostic indicator and functional modulator in breast cancer.Frontiers in oncology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The leucine-rich repeat containing protein (NLR) canonical inflammasome family includes Nod-like receptor protein 3 (NLRP3). Via the mediation of apoptosis proteins and immunological reactions, it controls the pathogenesis of malignancy. Experimental studies showed a relationship among lymphogenesis, cancer metastasis, and NLRP3 expression. Natural products have also been used as lead-based substances in a number of investigations to speed up the creation of novel, specific NLRP3 inhibitors. Via the mediation of apoptotic proteins and immunological responses, it controls the pathogenesis of malignancy. Moreover, it was recently noted that among human cancers, chemotherapy activates NLRP3. Induction of NLRP3 could encourage the generation of IL-1β and IL-22 to facilitate the propagation of malignancy. Additionally, prior research has demonstrated that the usage of NLRP3 in cancer therapy may result in resistance to drugs. The depletion of NLRP3 could affect the survival of cells. Natural products have been used as lead materials in a number of studies to help generate novel, specific NLRP3 antagonists more quickly. In the present review, we examine the mechanism behind the beneficial effects of the natural substances on the inhibition of cancer growth and progression, with special focus on NLRP3 regulation.
Indexed as
Identifiers
40116873What OpenQuestion holds
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.