Evidence map›Paper›PMID 19266252›Full record

ReviewClinical and experimental nephrology2009

Slit diaphragm dysfunction in proteinuric states: identification of novel therapeutic targets for nephrotic syndrome.

Hiroshi Kawachi, Koichi Suzuki, Naoko Miyauchi, Taeko Hashimoto, Yasuhiro Otaki, Fujio Shimizu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical and experimental nephrology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. A zebrafish model of congenital nephrotic syndrome of the Finnish type.Frontiers in cell and developmental biology · 2022
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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

6 authors at 3 institutions in 1 country.

Hiroshi KawachiDepartment of Cell Biology, Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Niigata, 951-8510, Japan. kawachi@med.niigata-u.ac.jp.
Koichi SuzukiDepartment of Cell Biology, Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Niigata, 951-8510, Japan.
Naoko MiyauchiDepartment of Cell Biology, Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Niigata, 951-8510, Japan.
Taeko HashimotoDepartment of Cell Biology, Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Niigata, 951-8510, Japan.
Yasuhiro OtakiDepartment of Cell Biology, Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Niigata, 951-8510, Japan.
Fujio ShimizuNiigata Seiryo University, Niigata, Japan.
Niigata University Medical and Dental Hospital · JPNiigata University · JPNiigata Seiryo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several recent studies have demonstrated that the slit diaphragm of the glomerular epithelial cell (podocyte) is the structure likely to be the principal barrier in the glomerular capillary wall. Nephrin identified as a gene product mutated in congenital nephrotic syndrome located at the outer leaflet of plasma membranes of the slit diaphragm. The anti-nephrin antibody is capable of inducing massive proteinuria, which indicates that nephrin is a key functional molecule in the slit diaphragm. Expression of nephrin was reduced in glomeruli of minimal change nephrotic syndrome. Some recent studies demonstrated that podocin, CD2-associated protein and NEPH1 are also functional molecules in the slit diaphragm, and their expressions are altered in membranous nephropathy and also in focal glomerulosclerosis. These observations suggested that the alteration of the molecular arrangement in the slit diaphragm is involved in the development of proteinuria in several kinds of glomerular diseases. Recent studies of our group have demonstrated that type 1 receptor-mediated angiotensin II action reduced the expression of the slit diaphragm-associated molecules and that type 1 receptor blockade ameliorated proteinuria by preventing the function of angiotensin II on the slit diaphragm. By the subtraction hybridization techniques using glomerular cDNA of normal and proteinuric rats, we detected that synaptic vesicle protein 2B and ephrin B1 are involved in the maintenance of the barrier function of the slit diaphragm.

Indexed as

Glomerular Filtration RateAdaptor Proteins, Signal TransducingAngiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsCytoskeletal ProteinsEphrin-B1HumansIntracellular Signaling Peptides and ProteinsMembrane GlycoproteinsMembrane ProteinsNephrotic SyndromeNerve Tissue ProteinsPodocytesProteinuriaReceptor, Angiotensin, Type 1Adaptor Proteins, Signal TransducingAngiotensin IIAngiotensin II Type 1 Receptor BlockersCD2-associated proteinCytoskeletal ProteinsEphrin-B1Intracellular Signaling Peptides and ProteinsMembrane GlycoproteinsMembrane ProteinsnephrinNerve Tissue ProteinsNPHS2 proteinReceptor, Angiotensin, Type 1Sv2b protein, rat

Identifiers

PMID19266252
OpenAlexW1973925742

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.