Evidence map›Paper›PMID 34431499›Full record

ArticleDisease models & mechanisms2021

Transforming growth factor β3 deficiency promotes defective lipid metabolism and fibrosis in murine kidney.

Elia Escasany, Borja Lanzón, Almudena García-Carrasco, Adriana Izquierdo-Lahuerta, Lucía Torres, Patricia Corrales, Ana Elena Rodríguez Rodríguez, Sergio Luis-Lima, Concepción Martínez Álvarez, Francisco Javier Ruperez and 4 more

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.4field-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

14 citing papers in PubMed, 25 citations in OpenAlex.

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  11. The Role of TGF-β3 in Radiation Response.International journal of molecular sciences · 2023
    Review
  12. Article
  13. What lies beyond 100 years of insulin.Disease models & mechanisms · 2021
    Article
  14. 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

14 authors at 7 institutions in 2 countries.

Elia EscasanyLipobeta group, Área de Bioquímica y Biología Molecular, Departamento de Ciencias Básicas de la Salud, Facultad de Ciencias de la Salud, Universidad Rey Juan Carlos, Avda. de Atenas s/n, Alcorcón, 28922 Madrid, Spain.
Borja LanzónLipobeta group, Área de Bioquímica y Biología Molecular, Departamento de Ciencias Básicas de la Salud, Facultad de Ciencias de la Salud, Universidad Rey Juan Carlos, Avda. de Atenas s/n, Alcorcón, 28922 Madrid, Spain.
Almudena García-CarrascoLipobeta group, Área de Bioquímica y Biología Molecular, Departamento de Ciencias Básicas de la Salud, Facultad de Ciencias de la Salud, Universidad Rey Juan Carlos, Avda. de Atenas s/n, Alcorcón, 28922 Madrid, Spain.
Adriana Izquierdo-LahuertaLipobeta group, Área de Bioquímica y Biología Molecular, Departamento de Ciencias Básicas de la Salud, Facultad de Ciencias de la Salud, Universidad Rey Juan Carlos, Avda. de Atenas s/n, Alcorcón, 28922 Madrid, Spain.
Lucía TorresLipobeta group, Área de Bioquímica y Biología Molecular, Departamento de Ciencias Básicas de la Salud, Facultad de Ciencias de la Salud, Universidad Rey Juan Carlos, Avda. de Atenas s/n, Alcorcón, 28922 Madrid, Spain.
Patricia CorralesLipobeta group, Área de Bioquímica y Biología Molecular, Departamento de Ciencias Básicas de la Salud, Facultad de Ciencias de la Salud, Universidad Rey Juan Carlos, Avda. de Atenas s/n, Alcorcón, 28922 Madrid, Spain.
Ana Elena Rodríguez RodríguezHospital Universitario de las Islas Canarias, Unidad de Investigación, 38320 La Laguna, Tenerife, Spain.ORCID 0000-0002-0803-864X
Sergio Luis-LimaIIS-Fundación Jiménez Díaz, Departamento de Nefrología e Hipertensión, 28040 Madrid, Spain.ORCID 0000-0003-3540-8252
Concepción Martínez ÁlvarezDepartamento de Anatomía y Embriología, Facultad de Medicina, Universidad Complutense de Madrid, 28040 Madrid, Spain.
Francisco Javier RuperezCentro de Metabolómica y Bioanálisis (CEMBIO), Facultad de Farmacia, Universidad San Pablo-CEU, CEU Universities, Urbanización Montepríncipe, Boadilla del Monte, 28660 Madrid, Spain.
Manuel RosLipobeta group, Área de Bioquímica y Biología Molecular, Departamento de Ciencias Básicas de la Salud, Facultad de Ciencias de la Salud, Universidad Rey Juan Carlos, Avda. de Atenas s/n, Alcorcón, 28922 Madrid, Spain.
Esteban PorriniUniversidad La Laguna, Instituto Tecnologías Biomédicas (ITB), 38200 La Laguna, Tenerife, Spain.ORCID 0000-0002-3056-4662
Mikael RydénDepartment of Medicine, Karolinska Institutet, Karolinska University Hospital, Huddinge, 141 86 Stockholm, Sweden.ORCID 0000-0003-4785-1876
Gema Medina-GómezLipobeta group, Área de Bioquímica y Biología Molecular, Departamento de Ciencias Básicas de la Salud, Facultad de Ciencias de la Salud, Universidad Rey Juan Carlos, Avda. de Atenas s/n, Alcorcón, 28922 Madrid, Spain.ORCID 0000-0001-8169-681X
Universidad Rey Juan Carlos · ESHospital Universitario de Canarias · ESHospital Universitario Fundación Jiménez Díaz · ESKarolinska University Hospital · SEUniversidad Complutense de Madrid · ESUniversidad de La Laguna · ESUniversidad San Pablo CEU · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glomerulosclerosis and tubulointerstitial fibrosis are pathological features of chronic kidney disease. Transforming growth factor β (TGFβ) is a key player in the development of fibrosis. However, of the three known TGFβ isoforms, only TGFβ1 has an established role in fibrosis, and the pathophysiological relevance of TGFβ2 and TGFβ3 is unknown. Because Tgfb3 deficiency in mice results in early postnatal lethality, we analyzed the kidney phenotype of heterozygous Tgfb3-knockout mice (Tgfb3+/-) and compared it with that of matched wild-type mice. Four-month-old Tgfb3+/- mice exhibited incipient renal fibrosis with epithelial-mesenchymal transition, in addition to glomerular basement membrane thickening and podocyte foot process effacement associated with albuminuria. Also evident was insulin resistance and oxidative stress at the renal level, together with aberrant renal lipid metabolism and mitochondrial function. Omics analysis revealed toxic species, such as diacylglycerides and ceramides, and dysregulated mitochondrial metabolism in Tgfb3+/- mice. Kidneys of Tgfb3+/- mice showed morphological alterations of mitochondria and overactivation of non-canonical MAPK ERK1/2 and JNK cascades. Our study indicates that renal TGFβ3 might have antifibrotic and renoprotective properties, opposing or counteracting the activity of TGFβ1. This article has an associated First Person interview with the first author of the paper.

Indexed as

Lipid MetabolismAnimalsFibrosisKidneyMiceMice, KnockoutTransforming Growth Factor betaTransforming Growth Factor beta1Transforming Growth Factor beta3Tgfb3 protein, mouseTransforming Growth Factor betaTransforming Growth Factor beta1Transforming Growth Factor beta3CKDFibrosisLipid metabolismMitochondriaOmicsTGFβ

Identifiers

PMID34431499
PMCPMC8489029
OpenAlexW3195518207

What OpenQuestion holds

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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.