Evidence map›Paper›PMID 35563876›Full record

ReviewCells2022

Genetic Kidney Diseases (GKDs) Modeling Using Genome Editing Technologies.

Fernando Gómez-García, Raquel Martínez-Pulleiro, Noa Carrera, Catarina Allegue, Miguel A Garcia-Gonzalez

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Genome editing and kidney health.Clinical kidney journal · 2024
    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

5 authors at 3 institutions in 1 country.

Fernando Gómez-GarcíaLaboratorio de Nefroloxía (No. 11), Grupo de Xenética e Bioloxía do Desenvolvemento das Enfermidades Renais, Instituto de Investigación Sanitaria de Santiago (IDIS), Complexo Hospitalario de Santiago de Compostela (CHUS), 15706 Santiago de Compostela, Spain.ORCID 0000-0002-7734-1896
Raquel Martínez-PulleiroLaboratorio de Nefroloxía (No. 11), Grupo de Xenética e Bioloxía do Desenvolvemento das Enfermidades Renais, Instituto de Investigación Sanitaria de Santiago (IDIS), Complexo Hospitalario de Santiago de Compostela (CHUS), 15706 Santiago de Compostela, Spain.ORCID 0000-0002-6039-5935
Noa CarreraLaboratorio de Nefroloxía (No. 11), Grupo de Xenética e Bioloxía do Desenvolvemento das Enfermidades Renais, Instituto de Investigación Sanitaria de Santiago (IDIS), Complexo Hospitalario de Santiago de Compostela (CHUS), 15706 Santiago de Compostela, Spain.ORCID 0000-0003-0739-0382
Catarina AllegueGrupo de Medicina Xenómica, Centro Singular de Investigación en Medicina Molecular y Enfermedades Crónicas (CiMUS), 15706 Santiago de Compostela, Spain.ORCID 0000-0002-5121-3159
Miguel A Garcia-GonzalezLaboratorio de Nefroloxía (No. 11), Grupo de Xenética e Bioloxía do Desenvolvemento das Enfermidades Renais, Instituto de Investigación Sanitaria de Santiago (IDIS), Complexo Hospitalario de Santiago de Compostela (CHUS), 15706 Santiago de Compostela, Spain.ORCID 0000-0002-4330-7200
Center for Research in Molecular Medicine and Chronic Diseases · ESFundación Pública Galega de Medicina Xenómica · ESInstituto de Investigación Sanitaria de Santiago · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic kidney diseases (GKDs) are a group of rare diseases, affecting approximately about 60 to 80 per 100,000 individuals, for which there is currently no treatment that can cure them (in many cases). GKDs usually leads to early-onset chronic kidney disease, which results in patients having to undergo dialysis or kidney transplant. Here, we briefly describe genetic causes and phenotypic effects of six GKDs representative of different ranges of prevalence and renal involvement (ciliopathy, glomerulopathy, and tubulopathy). One of the shared characteristics of GKDs is that most of them are monogenic. This characteristic makes it possible to use site-specific nuclease systems to edit the genes that cause GKDs and generate in vitro and in vivo models that reflect the genetic abnormalities of GKDs. We describe and compare these site-specific nuclease systems (zinc finger nucleases (ZFNs), transcription activator-like effect nucleases (TALENs) and regularly clustered short palindromic repeat-associated protein (CRISPR-Cas9)) and review how these systems have allowed the generation of cellular and animal GKDs models and how they have contributed to shed light on many still unknown fields in GKDs. We also indicate the main obstacles limiting the application of these systems in a more efficient way. The information provided here will be useful to gain an accurate understanding of the technological advances in the field of genome editing for GKDs, as well as to serve as a guide for the selection of both the genome editing tool and the gene delivery method most suitable for the successful development of GKDs models.

Indexed as

Gene EditingKidney DiseasesAnimalsCRISPR-Cas SystemsEndonucleasesFemaleHumansMaleZinc Finger NucleasesEndonucleasesZinc Finger NucleasesCRISPR-Cas9disease modelingGenetic kidney diseasesGKDs modelsTALENZFN

Identifiers

PMID35563876
PMCPMC9105797
OpenAlexW4229003634

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.