Evidence map›Paper›PMID 35037466›Full record

ArticleAmerican journal of physiology. Renal physiology2022

Metabolic reprogramming in a slowly developing orthologous model of polycystic kidney disease.

Katharina Hopp, Emily K Kleczko, Berenice Y Gitomer, Michel Chonchol, Jost Klawitter, Uwe Christians, Jelena Klawitter

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Observational
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Intestinal barrier function declines during polycystic kidney disease progression.American journal of physiology. Renal physiology · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. The AKI-to-CKD Transition: The Role of Uremic Toxins.International journal of molecular sciences · 2023
    Review
  18. Article
  19. Characterizing the metabolic response of the zebrafish kidney to overfeeding.American journal of physiology. Renal physiology · 2023
    Article
  20. Article
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

7 authors at 1 institution in 1 country.

Katharina HoppDivision of Renal Diseases and Hypertension, Department of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, Colorado.ORCID 0000-0002-2420-2358
Emily K KleczkoDivision of Renal Diseases and Hypertension, Department of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, Colorado.
Berenice Y GitomerDivision of Renal Diseases and Hypertension, Department of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, Colorado.
Michel ChoncholDivision of Renal Diseases and Hypertension, Department of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, Colorado.
Jost KlawitterDepartment of Anesthesiology, University of Colorado, Anschutz Medical Campus, Aurora, Colorado.
Uwe ChristiansDepartment of Anesthesiology, University of Colorado, Anschutz Medical Campus, Aurora, Colorado.
Jelena KlawitterDivision of Renal Diseases and Hypertension, Department of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, Colorado.
University of Colorado Anschutz Medical Campus · US

Funding

TRAINING IN RENAL &ELECTROLYTE DISEASE &HYPERTENSIONT32DK007135 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI JOHNSON, RICHARD JOSEPH, KENDRICK, JESSICA B · 1986 to 2024
$5.3M
Defining the functional role of T-cells in Autosomal Dominant Polycystic Kidney Disease pathologyK01DK114164 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI HOPP, KATHARINA · 2018 to 2022
$783k
The role of inflammation in the progression of polycystic kidney diseaseR01DK114424 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI GITOMER, BERENICE YOLANDE, KLAWITTER, JELENA · 2018 to 2020
$668k
HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) 5T32DK007135HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) DK114164HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) DK114424-03S1NIDDK NIH HHS K01 DK114164NIDDK NIH HHS R01 DK114424NIDDK NIH HHS T32 DK007135
6 · The paper itself

Abstract

Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disease and affects 1 in 1,000 individuals. There is accumulating evidence suggesting that there are shared cellular mechanisms responsible for cystogenesis in human and murine PKD and that reprogramming of metabolism is a key disease feature. In this study, we used a targeted metabolomics approach in an orthologous mouse model of PKD (

Indexed as

Energy MetabolismMutationAnimalsDatabases, GeneticDisease Models, AnimalDisease ProgressionGenetic Predisposition to DiseaseKidneyMetabolomeMetabolomicsMiceMice, Inbred C57BLMice, Mutant StrainsPhenotypePolycystic Kidney, Autosomal DominantTandem Mass SpectrometryTRPP Cation Channelsautosomal dominant polycystic kidney diseasekidney-gut axismetabolomicstryptophan metabolism

Identifiers

PMID35037466
PMCPMC8858679
OpenAlexW4206107451

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.