Evidence map›Paper›PMID 39350520›Full record

ArticleNephrology (Carlton, Vic.)2024

Renin-angiotensin blockade ameliorates the progression of glomerular injury in podocyte-specific Ctcf knockout mice.

Keisuke Fujioka, Takashi Nagai, Tomoki Hattori, Shoji Kagami, Koji Yasutomo, Niels Galjart, Teruyoshi Hirayama, Hiroshi Kawachi, Maki Urushihara

Abstract read
In one paragraph

Article in Nephrology (Carlton, Vic.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Keisuke FujiokaDepartment of Pediatrics, Institute of Health Biosciences, The Tokushima University Graduate School, Tokushima, Japan.
Takashi NagaiDepartment of Pediatrics, Institute of Health Biosciences, The Tokushima University Graduate School, Tokushima, Japan.
Tomoki HattoriDepartment of Pediatrics, Institute of Health Biosciences, The Tokushima University Graduate School, Tokushima, Japan.
Shoji KagamiDepartment of Pediatrics, Institute of Health Biosciences, The Tokushima University Graduate School, Tokushima, Japan.
Koji YasutomoDepartment of Immunology and Parasitology, Graduate School of Medicine, Tokushima University, Tokushima, Japan.
Niels GaljartDepartment of Cell Biology, Erasmus University Medical Center, Rotterdam, The Netherlands.
Teruyoshi HirayamaDepartment of Anatomy and Developmental Neurobiology, Tokushima University Graduate School of Medical Sciences, Tokushima, Japan.
Hiroshi KawachiDepartment of Cell Biology, Kidney Research Center, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Maki UrushiharaDepartment of Pediatrics, Institute of Health Biosciences, The Tokushima University Graduate School, Tokushima, Japan.ORCID https://orcid.org/0000-0002-6431-3239

Funding

Japan Society for the Promotion of Science 20K08181
6 · The paper itself

Abstract

aimSeveral studies have shown that the progression of proteinuria and renal tissue injury is associated with activation of the intrarenal renin-angiotensin system (RAS). CCCTC-binding factor (CTCF) is a DNA-binding factor that plays an essential role in the regulation of gene expression. In the present study, we aimed to investigate the phenotypic effects of CTCF deficiency in podocytes.

methodsAngiotensin II type 1 receptor blockers (ARBs) were administered to the podocyte-specific Ctcf knockout mice, and histological and biochemical analyzes were performed. We also investigated the changes in the expression of podocin in podocyte cell cultures with or without stimulation with angiotensin II from glomeruli isolated using magnetic beads from podocyte-specific Ctcf knockout mice.

resultsMice in which Ctcf was deleted from podocytes developed glomerulopathy and mice developed severe progressive proteinuria, and impaired renal function. Moreover, ARBs suppressed the development of glomerulopathy in podocyte-specific Ctcf knockout mice. Both real-time polymerase chain reaction and western blotting showed that podocin expression was decreased in cell cultures stimulated with angiotensin II. Furthermore, RAS components gene expressions in podocyte cell cultures isolated from podocyte-specific Ctcf knockout mice were significantly increased.

conclusionThese results suggest that RAS is involved in the development of glomerulopathy in podocyte-specific Ctcf knockout mice. Elucidation of the pathophysiology of podocyte-specific Ctcf knockout mice may provide new insights into the relationship between podocyte injury and chronic glomerulonephritis.

Indexed as

Angiotensin II Type 1 Receptor BlockersCCCTC-Binding FactorDisease Models, AnimalDisease ProgressionMice, KnockoutPodocytesProteinuriaRenin-Angiotensin SystemAngiotensin IIAnimalsCells, CulturedIntracellular Signaling Peptides and ProteinsKidney GlomerulusMaleMembrane ProteinsMiceAngiotensin IIAngiotensin II Type 1 Receptor BlockersCCCTC-Binding FactorCtcf protein, mouseIntracellular Signaling Peptides and ProteinsMembrane ProteinsNPHS2 proteinCCCTC‐binding factorknockout micenephritispodocyterenin‐angiotensin system

Identifiers

PMID39350520
PMCPMC13546959

What Socratic 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 Socratic graph.