ReviewNephron2023
CRRT 2023 Meeting: Targeting Amino Acid Transport to Improve Acute Kidney Injury Outcome.
Review in Nephron, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Integration of mitochondrial gene expression and immune landscape in acute kidney injury prediction.Renal failure · 2025Article
- Y665F variant of mouse Stat5b protects against acute kidney injury through transcriptomic shifts in renal gene expression.Scientific reports · 2025Article
- sc2DAT: workflow for targeting tumor subpopulations of single cells.Bioinformatics advances · 2025Article
- Western diet exacerbates a murine model of Balkan nephropathy.American journal of physiology. Renal physiology · 2025Article
- Metabolomic and transcriptomic insights into the mechanisms of renal ischemia-reperfusion injury progression.Scientific reports · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIn acute kidney injury (AKI), proximal tubules are a primary site of injury, resulting in significant alterations in amino acid transport and metabolism. However, little is known about the therapeutic potential of targeting amino acid transporters. Here, we briefly review the first experimental evidence that targeting the sodium-coupled amino acid transporter SLC6A19 (B0AT1) can improve AKI outcome. SUMMARY: SLC6A19 is expressed in the small intestine and early proximal tubules, where it absorbs and reabsorbs most of the ingested and filtered neutral amino acids, respectively. Systemic SLC6A19 deficiency alleviates renal cellular senescence and suppresses subsequent inflammation and fibrosis in a murine model of aristolochic acid-induced nephropathy, which targets the proximal tubule. The underlying mechanisms remain to be determined, but potentially may include reduced tubular workload, an inhibitory effect on SGLT2, downstream shift in transport and preconditioning of late proximal tubules, and induction of a fasting-like phenotype and lowering tubular accumulation of branched-chain amino acids, which all can promote tubular health.
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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.