ArticleInternational urology and nephrology2022
Cystine crystal-induced reactive oxygen species associated with NLRP3 inflammasome activation: implications for the pathogenesis of cystine calculi.
Article in International urology and nephrology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 3 citations in OpenAlex.
- Cell death‑related molecules and targets in the progression of urolithiasis (Review).International journal of molecular medicine · 2024Review
- Porous Se@SiOTranslational andrology and urology · 2024Article
- Protective Effect of Alkaline Mineral Water on Calcium Oxalate-Induced Kidney Injury in Mice.Evidence-based complementary and alternative medicine : eCAM · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
purposeTo investigate whether cystine crystal-induced production of reactive oxygen species (ROS) and activation of NLRP3 inflammasome contribute to cystine calculi formation.
methodsSlc7a9-knockout rats were created as cystine calculi animal models. Kidney histological examination using TEM and immunohistochemistry were performed. The protein expression of NLRP3 and IL-1β and the concentrations of oxidative stress markers such as ROS, MDA and H2O2 in kidney tissues were estimated. In parallel, HK-2 human renal proximal tubule cells were exposed to cystine crystals and NAC treatment. The protein and mRNA expression levels of NLRP3 were evaluated. Finally, cell apoptosis and cystine crystal adherence were also assessed.
resultsActivation of the NLRP3 inflammasome and marked elevations in MDA, H2O2 and ROS levels were observed both in vivo and in vitro. In particular, the protein and mRNA expression of NLRP3 was significantly increased by cystine crystals, but could be restored by an inhibitor of ROS. In addition, cell apoptosis and cystine crystal adherence were promoted by the NLRP3 inflammasome. The expression of CD44, OPN and HA in HK-2 cells was markedly increased by cystine crystals, but could be decreased by NLRP3 siRNA treatment.
conclusionNotably, we found that the activation of NLRP3 by cystine crystal-induced ROS production was of major importance in the pathogenesis of cystine calculi formation.
Indexed as
Identifiers
What 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.