ReviewNephron2016
Targeting Glycosphingolipid Metabolism to Treat Kidney Disease.
Review in Nephron, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 27 citations in OpenAlex.
- Venglustat, an orally administered glucosylceramide synthase inhibitor: Assessment over 3 years in adult males with classic Fabry disease in an open-label phase 2 study and its extension study.Molecular genetics and metabolism · 2023Trial
- Chronic kidney disease induces a distinct lipidomic signature and accelerates atherosclerosis progression in a novel minipig model.Laboratory animal research · 2026Article
- Spatial metabolomics and multiomics integration for breakthroughs in precision medicine for kidney disease.Nature reviews. Nephrology · 2026Review
- Imaging and spatially resolved mass spectrometry applications in nephrology.Nature reviews. Nephrology · 2025Review
- Sphingolipid Analysis in Clinical Research.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Lipidomic Profiling of Kidney Cortical Tubule Segments Identifies Lipotypes with Physiological Implications.Function (Oxford, England) · 2024Article
- GLP-1 Receptor Agonist Improves Mitochondrial Energy Status and Attenuates Nephrotoxicity In Vivo and In Vitro.Metabolites · 2023Article
- Adiposomes from Obese-Diabetic Individuals Promote Endothelial Dysfunction and Loss of Surface Caveolae.Cells · 2023Article
- Unraveling the Crosstalk between Lipids and NADPH Oxidases in Diabetic Kidney Disease.Pharmaceutics · 2023Review
- Review
- Article
- A Three-Metabolic-Genes Risk Score Model Predicts Overall Survival in Clear Cell Renal Cell Carcinoma Patients.Frontiers in oncology · 2020Article
- Sphingolipids and Diagnosis, Prognosis, and Organ Damage in Systemic Lupus Erythematosus.Frontiers in immunology · 2020Review
- Druggable Sphingolipid Pathways: Experimental Models and Clinical Opportunities.Advances in experimental medicine and biology · 2020Review
- Targeting glycosphingolipid metabolism as a potential therapeutic approach for treating disease in female MRL/lpr lupus mice.PloS one · 2020Article
- Identification of metabolism-associated genes and pathways involved in different stages of clear cell renal cell carcinoma.Oncology letters · 2018Article
- Diastereomer-specific quantification of bioactive hexosylceramides from bacteria and mammals.Journal of lipid research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The enhanced expression of glucosylceramide-based glycosphingolipids (GSLs) is a hallmark of many forms of renal disease including diabetic nephropathy, polycystic kidney disease and renal cell carcinoma. A common feature of each of these renal disorders is the preference metabolism via aerobic glycolysis. While aerobic glycolysis is an inefficient way to generate ATP, aerobic glycolysis promotes the formation of substrates important for the production of biomass, including lipids, amino acids and nucleotides, through the pentose phosphate pathway. Two products that are essential for the synthesis of glucosylceramide and more complex GSLs are generated through the pentose phosphate pathway. These products are reducing equivalents in the form of NADPH and UDP-glucose. In experimental models of each of these disorders, inhibition of glucosylceramide synthase with eliglustat or related analogues reverses the disease phenotype suggesting that blocking GSL synthesis should be explored as a potential treatment strategy.
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.