Evidence map›Paper›PMID 37783445›Full record

ArticleKidney international2023

Hepatocyte nuclear factor 4α mediated quinolinate phosphoribosylltransferase (QPRT) expression in the kidney facilitates resilience against acute kidney injury.

Amanda J Clark, Marie Christelle Saade, Vamsidhara Vemireddy, Kyle Q Vu, Brenda Mendoza Flores, Valerie Etzrodt, Erin J Ciampa, Huihui Huang, Ayumi Takakura, Kambiz Zandi-Nejad and 2 more

Open access · greenAbstract read
In one paragraph

Article in Kidney international, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.9field-weighted citation impact, top 6% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Quinolinic acid metabolism may mitigate AKI to CKD transition.bioRxiv : the preprint server for biology · 2025
    Article
  7. Observational
  8. NADTrends in molecular medicine · 2025
    Review
  9. Article
  10. Article
  11. Review
  12. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 1 country.

Amanda J ClarkDivision of Nephrology, Department of Medicine, University of Texas Southwestern, Dallas, Texas, USA; Division of Nephrology, Department of Pediatrics, University of Texas Southwestern, Dallas, Texas, USA.
Marie Christelle SaadeDivision of Nephrology, Department of Medicine, University of Texas Southwestern, Dallas, Texas, USA.
Vamsidhara VemireddyDivision of Nephrology, Department of Medicine, University of Texas Southwestern, Dallas, Texas, USA.
Kyle Q VuDivision of Nephrology, Department of Medicine, University of Texas Southwestern, Dallas, Texas, USA.
Brenda Mendoza FloresDivision of Nephrology, Department of Medicine, University of Texas Southwestern, Dallas, Texas, USA.
Valerie EtzrodtDivision of Nephrology, Department of Medicine, University of Texas Southwestern, Dallas, Texas, USA.
Erin J CiampaDepartment of Anesthesia, Critical Care, and Pain Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.
Huihui HuangDivision of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.
Ayumi TakakuraRenal Division, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Kambiz Zandi-NejadDivision of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.
Zsuzsanna K ZsengellérDivision of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.
Samir M ParikhDivision of Nephrology, Department of Medicine, University of Texas Southwestern, Dallas, Texas, USA; Department of Pharmacology, University of Texas Southwestern, Dallas, Texas, USA. Electronic address: samir.parikh@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · USBeth Israel Deaconess Medical Center · USBrigham and Women's Hospital · USSouthwestern Medical Center · US

Funding

UT Southwestern Medical Center Simmons Comprehensive Cancer CenterP30CA142543 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI MELANIE H. COBB · 2010 to 2026
$53.7M
Pediatric Scientist Development Program (PSDP) [K12]K12HD000850 · NICHD · YALE UNIVERSITY · PI Sallie R. Permar · 1987 to 2026
$44.1M
UT Southwestern NORCP30DK127984 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI Jeff G McDonald · 2022 to 2026
$7.4M
The Aging Kidney: Chronic Injury, Impaired Functions and Clinical OutcomesR01AG027002 · NIA · TUFTS MEDICAL CENTER · PI PARIKH, SAMIR M, SARNAK, MARK J · 2005 to 2022
$7.3M
Tie2-driven vascular control in critical illnessR35HL139424 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI PARIKH, SAMIR M · 2018 to 2024
$6.4M
Mitochondrial Biogenesis in Kidney DiseaseR01DK095072 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI Samir M Parikh · 2012 to 2026
$5.3M
Spinning Disk Confocal for UT SouthwesternS10OD028630 · OD · UT SOUTHWESTERN MEDICAL CENTER · PI LUBY-PHELPS, KATHERINE J · 2020 to 2020
$600k
NCI NIH HHS P30 CA142543NHLBI NIH HHS R35 HL139424NIA NIH HHS R01 AG027002NICHD NIH HHS K12 HD000850NIDDK NIH HHS P30 DK127984NIDDK NIH HHS R01 DK095072NIH HHS S10 OD028630
6 · The paper itself

Abstract

Nicotinamide adenine dinucleotide (NAD+) levels decline in experimental models of acute kidney injury (AKI). Attenuated enzymatic conversion of tryptophan to NAD+ in tubular epithelium may contribute to adverse cellular and physiological outcomes. Mechanisms underlying defense of tryptophan-dependent NAD+ production are incompletely understood. Here we show that regulation of a bottleneck enzyme in this pathway, quinolinate phosphoribosyltransferase (QPRT) may contribute to kidney resilience. Expression of QPRT declined in two unrelated models of AKI. Haploinsufficient mice developed worse outcomes compared to littermate controls whereas novel, conditional gain-of-function mice were protected from injury. Applying these findings, we then identified hepatocyte nuclear factor 4 alpha (HNF4α) as a candidate transcription factor regulating QPRT expression downstream of the mitochondrial biogenesis regulator and NAD+ biosynthesis inducer PPARgamma coactivator-1-alpha (PGC1α). This was verified by chromatin immunoprecipitation. A PGC1α - HNF4α -QPRT axis controlled NAD+ levels across cellular compartments and modulated cellular ATP. These results propose that tryptophan-dependent NAD+ biosynthesis via QPRT and induced by HNF4α may be a critical determinant of kidney resilience to noxious stressors.

Indexed as

Acute Kidney InjuryQuinolinic AcidAnimalsHepatocyte Nuclear Factor 1-alphaHepatocyte Nuclear FactorsKidneyMiceNADNicotinate-Nucleotide Diphosphorylase (Carboxylating)Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaTryptophanHepatocyte Nuclear Factor 1-alphaHepatocyte Nuclear FactorsHnf1a protein, mouseNADNicotinate-Nucleotide Diphosphorylase (Carboxylating)Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaQuinolinic AcidTryptophanacute kidney injuryHNF4αmetabolismNAD

Identifiers

PMID37783445
PMCPMC10843022
OpenAlexW4387219651

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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 Socratic graph.