Evidence map›Paper›PMID 30459215›Full record

ReviewDisease models & mechanisms2018

Modeling epigenetic modifications in renal development and disease with organoids and genome editing.

Carmen Hurtado Del Pozo, Elena Garreta, Juan Carlos Izpisúa Belmonte, Nuria Montserrat

Open access · goldAbstract readReview
In one paragraph

Review in Disease models & mechanisms, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. The link among microbiota, epigenetics, and disease development.Environmental science and pollution research international · 2021
    Review
  2. Unraveling the epigenetic landscape of glomerular cells in kidney disease.Journal of molecular medicine (Berlin, Germany) · 2021
    Review
  3. Article
  4. Clinical Significance ofOncoTargets and therapy · 2021
    Article
  5. Epigenetics in kidney diseases.Advances in clinical chemistry · 2021
    Review
  6. Review
  7. Review
  8. Review
  9. Modeling congenital kidney diseases inDisease models & mechanisms · 2019
    Review
  10. Article
  11. 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

4 authors at 2 institutions in 2 countries.

Carmen Hurtado Del PozoPluripotency for organ regeneration. Institute for Bioengineering of Catalonia (IBEC), the Barcelona Institute of Technology (BIST), 08028 Barcelona, Spain.
Elena GarretaPluripotency for organ regeneration. Institute for Bioengineering of Catalonia (IBEC), the Barcelona Institute of Technology (BIST), 08028 Barcelona, Spain.
Juan Carlos Izpisúa BelmonteGene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037, USA belmonte@salk.edu nmontserrat@ibecbarcelona.eu.ORCID 0000-0003-0557-8875
Nuria MontserratPluripotency for organ regeneration. Institute for Bioengineering of Catalonia (IBEC), the Barcelona Institute of Technology (BIST), 08028 Barcelona, Spain belmonte@salk.edu nmontserrat@ibecbarcelona.eu.ORCID 0000-0002-1603-1755
Institute for Bioengineering of Catalonia · ESSalk Institute for Biological Studies · US

Funding

Evaluation of Regenerative Potential of Yamanaka Factors Against Renal DamageR21AG055938 · NIA · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI IZPISUA BELMONTE, JUAN CARLOS · 2017 to 2018
$534k
NIA NIH HHS R21 AG055938
6 · The paper itself

Abstract

Understanding epigenetic mechanisms is crucial to our comprehension of gene regulation in development and disease. In the past decades, different studies have shown the role of epigenetic modifications and modifiers in renal disease, especially during its progression towards chronic and end-stage renal disease. Thus, the identification of genetic variation associated with chronic kidney disease has resulted in better clinical management of patients. Despite the importance of these findings, the translation of genotype-phenotype data into gene-based medicine in chronic kidney disease populations still lacks faithful cellular or animal models that recapitulate the key aspects of the human kidney. The latest advances in the field of stem cells have shown that it is possible to emulate kidney development and function with organoids derived from human pluripotent stem cells. These have successfully recapitulated not only kidney differentiation, but also the specific phenotypical traits related to kidney function. The combination of this methodology with CRISPR/Cas9 genome editing has already helped researchers to model different genetic kidney disorders. Nowadays, CRISPR/Cas9-based approaches also allow epigenetic modifications, and thus represent an unprecedented tool for the screening of genetic variants, epigenetic modifications or even changes in chromatin structure that are altered in renal disease. In this Review, we discuss these technical advances in kidney modeling, and offer an overview of the role of epigenetic regulation in kidney development and disease.

Indexed as

Epigenesis, GeneticGene EditingModels, GeneticAnimalsHumansKidneyKidney DiseasesOrganoidsCRISPR/Cas9EpigeneticsGenome editingOrganoids

Identifiers

PMID30459215
PMCPMC6262817
OpenAlexW2901979880

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.