ReviewJournal of inherited metabolic disease2008
Membrane translocation of glutaric acid and its derivatives.
Review in Journal of inherited metabolic disease, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
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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.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Solute carrier transporters as metabolic gatekeepers in tumor-microenvironment crosstalk.Acta pharmacologica Sinica · 2026Review
- Transcriptome Sequencing and Metabolite Analysis Revealed the Single and Combined Effects of Microplastics and Di-(2-ethylhexyl) Phthalate on Mouse Liver.International journal of molecular sciences · 2025Article
- Both Enantiomers of 2-Hydroxyglutarate Modulate the Metabolism of Cultured Human Neuroblastoma Cells.Neurochemical research · 2024Article
- Cerebral White Matter Alterations Associated With Oligodendrocyte Vulnerability in Organic Acidurias: Insights in Glutaric Aciduria Type I.Neurotoxicity research · 2024Review
- SLC1A1-mediated cellular and mitochondrial influx of R-2-hydroxyglutarate in vascular endothelial cells promotes tumor angiogenesis in IDH1-mutant solid tumors.Cell research · 2022Article
- Lactonization of the Oncometabolite D-2-Hydroxyglutarate Produces a Novel Endogenous Metabolite.Cancers · 2021Article
- The Interplay Between the Genetic and Immune Landscapes of AML: Mechanisms and Implications for Risk Stratification and Therapy.Frontiers in oncology · 2019Review
- Suppression of antitumor T cell immunity by the oncometabolite (R)-2-hydroxyglutarate.Nature medicine · 2018Article
- Glutaric Aciduria Type 1 and Acute Renal Failure: Case Report and Suggested Pathomechanisms.JIMD reports · 2018Article
- Combined D2-/L2-hydroxyglutaric aciduria (SLC25A1 deficiency): clinical course and effects of citrate treatment.Journal of inherited metabolic disease · 2014Observational
- Glutaric Aciduria type I and acute renal failure - Coincidence or causality?Molecular genetics and metabolism reports · 2014Article
- Increased blood-brain barrier permeability and alterations in perivascular astrocytes and pericytes induced by intracisternal glutaric acid.Fluids and barriers of the CNS · 2014Article
- Glutaric aciduria type 1 metabolites impair the succinate transport from astrocytic to neuronal cells.The Journal of biological chemistry · 2011Article
- The sodium-dependent di- and tricarboxylate transporter, NaCT, is not responsible for the uptake of D-, L-2-hydroxyglutarate and 3-hydroxyglutarate into neurons.Journal of inherited metabolic disease · 2011Article
- False-positive newborn screening mimicking glutaric aciduria type I in infants with renal insufficiency.Journal of inherited metabolic disease · 2009Article
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 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The neurodegenerative disorder glutaric aciduria type I (GA I) is characterized by increased levels of cytotoxic metabolites such as glutaric acid (GA) and 3-hydroxyglutaric (3OHGA). The present report summarizes recent investigations providing insights into mechanisms of intra- and intercellular translocation of these metabolites. Initiated by microarray analyses in a mouse model of GA I, the sodium-dependent dicarboxylate cotransporter 3 (NaC3) was the first molecule identified to mediate the translocation of GA and 3OHGA with high and low affinity, respectively. More recently, organic anion transporters (OAT) 1 and 4 have been reported to be high-affinity transporters for GA and 3OHGA as well as D-2- and L-2-hydroxyglutaric acid (D2OHGA, L2OHGA). The concerted action of NaC3 and OATs may be important for the directed uptake and excretion of GA, 3OHGA, D2OHGA and L2OHGA in kidney proximal tubule cells. In addition, experimental data on cultured neuronal and glial cells isolated from mouse brain demonstrated that GA rather than 3OHGA may competitively inhibit the anaplerotic supply of tricarboxylic acid cycle intermediates from astrocytes to neurons. The identification of GA and GA derivative transporters may represent targets for new approaches to treat patients with GA I and related disorders.
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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.