Evidence mapPaperPMID 32438732Full record

ReviewInternational journal of molecular sciences2020

Revisiting Experimental Models of Diabetic Nephropathy.

Anna Giralt-López, Mireia Molina-Van den Bosch, Ander Vergara, Clara García-Carro, Daniel Seron, Conxita Jacobs-Cachá, Maria José Soler

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
7.3field-weighted citation impact, top 2% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
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  18. Effect ofInternational journal of molecular sciences · 2024
    Article
  19. Review
  20. Rodent models of AKI and AKI-CKD transition: an update in 2024.American journal of physiology. Renal physiology · 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

7 authors at 1 institution in 1 country.

Anna Giralt-LópezNephrology Research Group, Vall d'Hebrón Institut de Recerca, 08035 Barcelona, Spain.
Mireia Molina-Van den BoschNephrology Research Group, Vall d'Hebrón Institut de Recerca, 08035 Barcelona, Spain.
Ander VergaraNephrology Research Group, Vall d'Hebrón Institut de Recerca, 08035 Barcelona, Spain.
Clara García-CarroNephrology Research Group, Vall d'Hebrón Institut de Recerca, 08035 Barcelona, Spain.
Daniel SeronNephrology Research Group, Vall d'Hebrón Institut de Recerca, 08035 Barcelona, Spain.ORCID 0000-0003-2054-653X
Conxita Jacobs-CacháNephrology Research Group, Vall d'Hebrón Institut de Recerca, 08035 Barcelona, Spain.ORCID 0000-0003-3621-0766
Maria José SolerNephrology Research Group, Vall d'Hebrón Institut de Recerca, 08035 Barcelona, Spain.ORCID 0000-0003-2518-7847
Vall d'Hebron Institut de Recerca · ES

Funding

Instituto de Salud Carlos III PI17/00257Instituto de Salud Carlos III PI18/01704Instituto de Salud Carlos III RD16/0009/0030
6 · The paper itself

Abstract

Diabetes prevalence is constantly increasing and, nowadays, it affects more than 350 million people worldwide. Therefore, the prevalence of diabetic nephropathy (DN) has also increased, becoming the main cause of end-stage renal disease (ESRD) in the developed world. DN is characterized by albuminuria, a decline in glomerular filtration rate (GFR), hypertension, mesangial matrix expansion, glomerular basement membrane thickening, and tubulointerstitial fibrosis. The therapeutic advances in the last years have been able to modify and delay the natural course of diabetic kidney disease (DKD). Nevertheless, there is still an urgent need to characterize the pathways that are involved in DN, identify risk biomarkers and prevent kidney failure in diabetic patients. Rodent models provide valuable information regarding how DN is set and its progression through time. Despite the utility of these models, kidney disease progression depends on the diabetes induction method and susceptibility to diabetes of each experimental strain. The classical DN murine models (Streptozotocin-induced, Akita, or obese type 2 models) do not develop all of the typical DN features. For this reason, many models have been crossed to a susceptible genetic background. Knockout and transgenic strains have also been created to generate more robust models. In this review, we will focus on the description of the new DN rodent models and, additionally, we will provide an overview of the available methods for renal phenotyping.

Indexed as

AnimalsDiabetic NephropathiesDisease Models, AnimalGlomerular Filtration RateHumansKidneyPodocytesdiabetic nephropathyexperimental models of DNhistological lesionsrenal function

Identifiers

PMID32438732
PMCPMC7278948
OpenAlexW3027034303

What Socratic 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 Socratic graph.