ArticleMolecular medicine reports2021
Reactive oxygen species induced by uric acid promote NRK‑52E cell apoptosis through the NEK7‑NLRP3 signaling pathway.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Maternal hyperuricemia and adverse maternal-fetal outcomes: a systematic review and meta-analysis of observational studies.Frontiers in medicine · 2026Pooled it
- Article
- Article
- Uric acid-associated mechanisms of coronary artery calcification in diabetic kidney disease: evidence, hypotheses, and translational perspectives.Frontiers in cardiovascular medicine · 2026Review
- Relative Fat Mass Associated with Hyperuricemia in Adults: A Cross-Sectional Study.Endocrine, metabolic & immune disorders drug targets · 2026Article
- Research advances on NLRP3 inflammasomes in organ transplantation.Frontiers in immunology · 2026Review
- Deciphering the NEK7-NLRP3 inflammasome assembly: from conformational activation to allosteric drug discovery.Frontiers in immunology · 2026Review
- NEK Family Kinases: Structure, Function, and Role in Disease.Biomolecules · 2025Review
- Review
- Risk of Sudden Sensorineural Hearing Loss in Patients with Gout: A Population-Level Study in a South Korean National Health Screening Cohort.Journal of clinical medicine · 2025Article
- Mitophagy Regulates Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2024Review
- Wuling San Based on Network Pharmacology and in vivo Evidence Against Hyperuricemia via Improving Oxidative Stress and Inhibiting Inflammation.Drug design, development and therapy · 2023Article
- In Mitosis You Are Not: The NIMA Family of Kinases inInternational journal of molecular sciences · 2022Review
- Involvement of Inflammasome Components in Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Total extract ofFrontiers in pharmacology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing uric acid (UA) could induce renal tubular epithelial cell (NRK‑52E) injury. However, the specific mechanism by which UA induces renal tubular epithelial cell injury remains unknown. It was hypothesized that UA induces renal tubular epithelial cell injury through reactive oxygen species (ROS) and the Never in mitosis gene A (NIMA)‑related kinase 7 (NEK7)/NLR family pyrin domain containing 3 (NLRP3) signaling pathway. TUNEL assay and flow cytometry were applied to measure apoptosis, and the results of the present study showed that UA treatment induced apoptosis of NRK‑52E cells in a concentration‑dependent manner. Western blotting was performed to determine the expression levels of cleaved caspase‑3, Bax and Bcl‑xl, it was found that levels were significantly increased after UA treatment in NRK‑52E cells. ROS and apoptosis were predominantly induced in NRK‑52E cells and there was an association between ROS and apoptosis. Enhanced expression of NEK7, NLRP3, apoptosis‑associated speck‑like and caspase‑1 were observed in NRK‑52E cells treated with UA. The ROS inhibitor, N‑acetyl‑l‑cysteine, exerted a protective effect on the UA‑induced apoptosis of tubular epithelial cells by reducing excess ROS production, which significantly inhibited NEK7 and NLRP3 inflammasome activation. These results indicated that UA activates ROS and induces apoptosis of NRK‑52E cells. The mechanism might be related to the regulation of the NEK7/NLRP3 signaling pathway.
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.