ArticleClinical science (London, England : 1979)2018
Pharmacological inhibition of autophagy by 3-MA attenuates hyperuricemic nephropathy.
Article in Clinical science (London, England : 1979), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 85 citations in OpenAlex.
- Hyperuricemia increases susceptibility to chronic kidney injury exacerbation via autophagic flux blockade-mediated ammonia death pathway.Journal of advanced research · 2026Article
- Uric acid enhances tumor stemness in breast cancer cells by upregulating GMPS.Molecular medicine reports · 2026Article
- Antioxidant malic-acid-derived lipid nanoparticles delivering secretory uricase circRNA for hyperuricemia and complication management in mice.Nature communications · 2026Article
- Targeting programmed cell death: a novel therapeutic paradigm for cancer based on mode-of-death classification.Apoptosis : an international journal on programmed cell death · 2026Review
- Small molecules targeting regulated cell death for chronic kidney disease therapy.Journal of pharmaceutical analysis · 2026Review
- The Positive Feedback Loop of Hypoxia-Inducible Factor-1 α /miR-295/Factor Inhibiting Hypoxia-Inducible Factor-1 in Hyperuricemic Nephropathy.Kidney360 · 2026Article
- Roxadustat alleviates cisplatin-induced acute kidney injury by regulating fatty acid oxidation and mitochondrial function.Renal failure · 2025Article
- Molecular Basis of Oxidative Stress-Induced Acute Kidney Injury, Kidney Fibrosis, Chronic Kidney Disease, and Clinical Significance of Targeting Reactive Oxygen Species-Regulated Pathways to Treat Kidney Disease.Frontiers in bioscience (Scholar edition) · 2025Review
- Neferine Targeted the NLRC5/NLRP3 Pathway to Inhibit M1-type Polarization and Pyroptosis of Macrophages to Improve Hyperuricemic Nephropathy.Current molecular medicine · 2025Article
- Resveratrol activates autophagy and protects from UVA-induced photoaging in human skin fibroblasts and the skin of male mice by regulating the AMPK pathway.Biogerontology · 2024Article
- Review
- Autophagy inhibitor 3-methyladenine attenuates renal injury in streptozotocin-induced diabetic mice.Iranian journal of basic medical sciences · 2024Article
- The pro-fibrotic role of autophagy in renal intrinsic cells: mechanisms and therapeutic potential in chronic kidney disease.Frontiers in cell and developmental biology · 2024Review
- PDGFβ receptor-targeted delivery of truncated transforming growth factor β receptor type II for improving the in vitro and in vivo anti-renal fibrosis activity via strong inactivation of TGF-β1/Smad signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- The Function of Autophagy in the Initiation, and Development of Breast Cancer.Current medicinal chemistry · 2024Review
- Histone demethylase KDM4B contributes to advanced clear cell renal carcinoma and association with copy number variations and cell cycle progression.Epigenetics · 2023Article
- The effect of lipid metabolism disorder on patients with hyperuricemia using Multi-Omics analysis.Scientific reports · 2023Article
- Autophagy and Biomaterials: A Brief Overview of the Impact of Autophagy in Biomaterial Applications.Pharmaceutics · 2023Review
- Article
- Review
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 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy has been identified as a cellular process of bulk degradation of cytoplasmic components and its persistent activation is critically involved in the renal damage induced by ureteral obstruction. However, the role and underlying mechanisms of autophagy in hyperuricemic nephropathy (HN) remain unknown. In the present study, we observed that inhibition of autophagy by 3-methyladenine (3-MA) abolished uric acid-induced differentiation of renal fibroblasts to myofibroblasts and activation of transforming growth factor-β1 (TGF-β1), epidermal growth factor receptor (EGFR), and Wnt signaling pathways in cultured renal interstitial fibroblasts. Treatment with 3-MA also abrogated the development of HN
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.