ReviewMolecular biology reports2025
NLRP3 as a therapeutic target in cyclophosphamide-associated toxicities.
Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
6 citing papers in PubMed.
- Cardioprotective role of vincamine in cyclophosphamide-induced cardiotoxicity through modulation of AMPK/SIRT1, PI3K/Akt, and MAPK pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Febuxostat alleviates testicular dysfunction induced by cyclophosphamide in rats via modulation of pyroptosis and mTOR autophagy axis.Scientific reports · 2026Article
- 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
- Buspirone combats cyclophosphamide-provoked hepatotoxicity in rats via activation of AMPK/Nrf2/HO-1 and suppression of NF-κB p65 /NLRP3 inflammasome pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Mechanistic insights into the hepatoprotective role of rabeprazole against cyclophosphamide-induced hepatotoxicity via AMPK/SIRT1 activation and suppression of TLR4/NF-κB and MAPK pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Rapid and sensitive electrochemical detection of paracetamol using EuZrOScientific reports · 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclophosphamide (CPM), a potent chemotherapeutic agent, while effective against various cancers, can cause significant organ damage. The NLRP3 inflammasome, a key player in the innate immune response, is implicated in this toxicity. This review delves into the intricate relationship between CPM and NLRP3 inflammasome activation, focusing on oxidative stress-mediated organ damage. We explore the mechanisms by which CPM induces NLRP3 activation in the kidneys, heart, liver, and gastrointestinal tract. Additionally, we examine the signaling pathways involved in this process. The review also discusses potential therapeutic interventions, including phytotherapeutic agents, that target NLRP3 inflammasome activation to mitigate CPM-induced organ injury. By highlighting the crucial role of NLRP3 in CPM-related toxicity, this review provides a foundation for future research aimed at developing novel therapeutic strategies to minimize adverse effects and improve patient outcomes.
Indexed as
Identifiers
40192868What 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.