Evidence map›Paper›PMID 24464477›Full record

ReviewPediatric nephrology (Berlin, Germany)2014

Semaphorin3a signaling, podocyte shape, and glomerular disease.

Alda Tufro

Abstract readReview
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 41% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Novel Roles of GPCRs in the Renal Collecting Duct.Physiology (Bethesda, Md.) · 2026
    Review
  2. Article
  3. Article
  4. Role of Semaphorin 3A in Kidney Development and Diseases.Diagnostics (Basel, Switzerland) · 2023
    Review
  5. Article
  6. Semaphorin3A-Inhibitor Ameliorates Doxorubicin-Induced Podocyte Injury.International journal of molecular sciences · 2020
    Article
  7. Gpr97 Exacerbates AKI by Mediating Sema3A Signaling.Journal of the American Society of Nephrology : JASN · 2018
    Article
  8. Vascular Growth Factors and Glomerular Disease.Annual review of physiology · 2016
    Review
  9. Chronic allograft rejection: a fresh look.Current opinion in organ transplantation · 2015
    Review
  10. 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

1 author at 1 institution in 1 country.

Alda TufroDepartment of Pediatrics, Yale University School of Medicine, 333 Cedar Street, PO Box 208064, New Haven, CT, 06520-8064, USA, alda.tufro@yale.edu.
Yale University · US

Funding

Kidney Vascularization-- VEGF-mediated MechanismsR01DK059333 · NIDDK · YESHIVA UNIVERSITY · PI TUFRO, ALDA · 2001 to 2011
$2.9M
Kidney vascularization: semaphorin-mediated mechanisms.R01DK064187 · NIDDK · YESHIVA UNIVERSITY · PI TUFRO, ALDA · 2003 to 2006
$1.2M
Function of semaphorin3a in diabetic nephropathyR01DK098824 · NIDDK · YALE UNIVERSITY · PI TUFRO, ALDA · 2013 to 2016
$999k
NIDDK NIH HHS DK59333NIDDK NIH HHS DK64187NIDDK NIH HHS R01 DK059333NIDDK NIH HHS R01 DK064187NIDDK NIH HHS R01 DK098824
6 · The paper itself

Abstract

Semaphorin3a (sema3a), a member of class 3 semaphorins, is a guidance protein that regulates angiogenesis, branching morphogenesis, axon growth, and cell migration, and has pleiotropic roles on organogenesis, immune response, and cancer. Sema3a is secreted by podocytes and is required for normal kidney patterning and glomerular filtration barrier development. We recently discovered that after completion of kidney development, Sema3a gain-of-function in podocytes leads to proteinuric glomerular disease in mice. Excess sema3a causes foot process effacement, glomerular basement lamination, and endothelial damage in vivo, and disrupts cell autonomously podocyte shape by down-regulating nephrin and inhibiting αvβ3 integrin. We identified a novel direct interaction between nephrin and plexinA1, the sema3a signaling receptor. Nephrin-plexinA1 interaction links the slit-diaphragm signaling complex to extracellular sema3a signals. Hence, sema3a functions as an extracellular negative regulator of the structure and function of the glomerular filtration barrier.

Indexed as

AnimalsHumansKidneyKidney DiseasesOrganogenesisPodocytesSemaphorin-3ASignal TransductionSemaphorin-3A

Identifiers

PMID24464477
PMCPMC3992269
OpenAlexW2006605316

What OpenQuestion holds

Textmetadata
LicenceTDM
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.