Evidence map›Paper›PMID 35429495›Full record

ReviewKidney international2022

The impact of genetic background on mouse models of kidney disease.

Rei Bufi, Ron Korstanje

Open access · greenAbstract readReview
In one paragraph

Review in Kidney international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Contribution of murine strain background to NabioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Integrins in the kidney - beyond the matrix.Nature reviews. Nephrology · 2025
    Review
  9. Phenotype of Parathyroid-targetedJournal of the Endocrine Society · 2024
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. UMOD and the architecture of kidney disease.Pflugers Archiv : European journal of physiology · 2022
    Review
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

2 authors at 1 institution in 1 country.

Rei BufiThe Jackson Laboratory, Bar Harbor, Maine, USA.
Ron KorstanjeThe Jackson Laboratory, Bar Harbor, Maine, USA. Electronic address: ron.korstanje@jax.org.
Jackson Laboratory · US

Funding

Translational CoreP30AG038070 · NIA · JACKSON LABORATORY · PI John Matthew Mahoney · 2010 to 2026
$19.3M
Genetic Factors that Influence Arsenic ToxicityR01ES029916 · NIEHS · JACKSON LABORATORY · PI CHURCHILL, GARY A, KORSTANJE, RONNY · 2019 to 2023
$3.6M
Causal connections between axon guidance proteins and early progressive kidney function decline in diabetesR01DK131061 · NIDDK · JOSLIN DIABETES CENTER · PI KROLEWSKI, ANDRZEJ S · 2022 to 2025
$2.7M
Identification of Kidney Disease Modifier Genes in Mouse and Human Alport SyndromeR01DK131019 · NIDDK · JACKSON LABORATORY · PI KORSTANJE, RONNY · 2022 to 2025
$1.5M
NIA NIH HHS P30 AG038070NIDDK NIH HHS R01 DK131019NIDDK NIH HHS R01 DK131061NIEHS NIH HHS R01 ES029916
6 · The paper itself

Abstract

The mouse is the most commonly used mammalian model to study disease, including kidney disease. However, close attention needs to be paid to the differences and effects of genetic background. The default choice of most investigators is to use C57BL/6 mice, but not all C57BL/6 mice are the same. Ever since the C57BL/6 line was first established, differences in the genetic background have risen between substrains, which have major implications in the phenotypes expressed in kidney disease. Furthermore, considering that C57BL/6 substrains are relatively resistant to kidney damage, there can be major benefits in selecting other mouse inbred strains when studying kidney disease. These strains can show more similar responses regarding kidney damage as in humans, and results may therefore translate better to human application. Genetically diverse mice, such as the Diversity Outbred mice, allow investigators to study kidney phenotypes with comparable levels of genetic diversity as seen in humans, which yield results that more closely reflect the variation in human disease outcomes due to genetic variation. Hence, embracing the genetic diversity that is present in mice can lead to better translational research methods. Investigators need to always take into consideration that genetic background is a variable that can alter results significantly, and optimization of translational research asks for careful strain selection and more rigorous reporting of the genetic background that is being used in experiment.

Indexed as

Genetic BackgroundKidney DiseasesAnimalsDisease Models, AnimalGenetic VariationMammalsMiceMice, Inbred C57BLMice, Inbred StrainsSpecies Specificitygenetic backgroundgenetic diversitykidney diseasemouse modeltranslational research

Identifiers

PMID35429495
PMCPMC9233094
OpenAlexW4223925701

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.