Evidence map›Paper›PMID 29556761›Full record

ReviewClinical and experimental nephrology2018

Recent advances of animal model of focal segmental glomerulosclerosis.

Jae Won Yang, Anne Katrin Dettmar, Andreas Kronbichler, Heon Yung Gee, Moin Saleem, Seong Heon Kim, Jae Il Shin

Open access · hybridAbstract readReview
PubMed Publisher
In one paragraph

Review in Clinical and experimental nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Mechanisms of Scarring in Focal Segmental Glomerulosclerosis.Kidney diseases (Basel, Switzerland) · 2021
    Review
  17. Article
  18. Article
  19. Article
  20. Animal Models of Renal Pathophysiology and Disease.Methods in molecular biology (Clifton, N.J.) · 2021
    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 4 institutions in 3 countries.

Jae Won YangDepartment of Nephrology, Yonsei University Wonju College of Medicine, Wonju, Gangwon, Republic of Korea.
Anne Katrin DettmarPediatric Nephrology, Department of Pediatrics, Medical University Center Hamburg-Eppendorf, Hamburg, Germany.
Andreas KronbichlerDepartment of Internal Medicine IV (Nephrology and Hypertension), Universitätskliniken Innsbruck, Anichstraße 35, 6020, Innsbruck, Austria.
Heon Yung GeeDepartment of Pharmacology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Moin SaleemPaediatric Renal Medicine, University of Bristol, Bristol, UK.
Seong Heon Kim *Department of Pediatrics, Pusan National University Children's Hospital, Yangsan, Republic of Korea. pedksh@gmail.com.
Jae Il Shin *Department of Pediatrics, Yonsei University College of Medicine, 50 Yonsei-Ro, Seodaemun-gu, Seoul, 120-752, Republic of Korea. shinji@yuhs.ac.
Yonsei University · KRPusan National University Yangsan Hospital · KRUniversität Hamburg · DEUniversity of Bristol · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the last decade, great advances have been made in understanding the genetic basis for focal segmental glomerulosclerosis (FSGS). Animal models using specific gene disruption of the slit diaphragm and cytoskeleton of the foot process mirror the etiology of the human disease. Many animal models have been developed to understand the complex pathophysiology of FSGS. Therefore, we need to know the usefulness and exact methodology of creating animal models. Here, we review classic animal models and newly developed genetic animal models. Classic animal models of FSGS involve direct podocyte injury and indirect podocyte injury due to adaptive responses. However, the phenotype depends on the animal background. Renal ablation and direct podocyte toxin (PAN, adriamycin) models are leading animal models for FSGS, which have some limitations depending on mice background. A second group of animal models were developed using combinations of genetic mutation and toxin, such as NEP25, diphtheria toxin, and Thy1.1 models, which specifically injure podocytes. A third group of animal models involves genetic engineering techniques targeting podocyte expression molecules, such as podocin, CD2-associated protein, and TRPC6 channels. More detailed information about podocytopathy and FSGS can be expected in the coming decade. Different animal models should be used to study FSGS depending on the specific aim and sometimes should be used in combination.

Indexed as

Disease Models, AnimalGlomerulosclerosis, Focal SegmentalMutationAnimalsHumansKidney GlomerulusMicePodocytesAnimal modelFocal segmental glomerulosclerosisPodocyte

Identifiers

PMID29556761
OpenAlexW2792416359

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.