Evidence map›Paper›PMID 32220420›Full record

ArticleThe American journal of pathology2020

Loss of Roundabout Guidance Receptor 2 (Robo2) in Podocytes Protects Adult Mice from Glomerular Injury by Maintaining Podocyte Foot Process Structure.

Anna Pisarek-Horowitz, Xueping Fan, Sudhir Kumar, Hila M Rasouly, Richa Sharma, Hui Chen, Kathryn Coser, Crystal T Bluette, Dinesh Hirenallur-Shanthappa, Sarah R Anderson and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2020. 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
0.8field-weighted citation impact, top 29% 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, 21 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025
    Review
  6. Article
  7. Article
  8. Precision medicine for focal segmental glomerulosclerosis.Kidney research and clinical practice · 2024
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. 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

17 authors at 2 institutions in 1 country.

Anna Pisarek-HorowitzRenal Section, Department of Medicine, Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts.
Xueping FanRenal Section, Department of Medicine, Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts.
Sudhir KumarRenal Section, Department of Medicine, Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts.
Hila M RasoulyRenal Section, Department of Medicine, Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts.
Richa SharmaRenal Section, Department of Medicine, Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts.
Hui ChenDepartment of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts.
Kathryn CoserCenters for Therapeutic Innovation, Pfizer Inc., Cambridge, Massachusetts.
Crystal T BluetteComparative Medicine, Pfizer Inc., Cambridge, Massachusetts.
Dinesh Hirenallur-ShanthappaComparative Medicine, Pfizer Inc., Cambridge, Massachusetts.
Sarah R AndersonGlobal Pathology, Drug Safety Research and Development, Pfizer Inc., Groton, Connecticut.
Hongying YangCenters for Therapeutic Innovation, Pfizer Inc., Cambridge, Massachusetts.
Laurence H BeckRenal Section, Department of Medicine, Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts.
Ramon G BonegioRenal Section, Department of Medicine, Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts.
Joel M HendersonDepartment of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts.
Stephen P BerasiCenters for Therapeutic Innovation, Pfizer Inc., Cambridge, Massachusetts.
David J SalantRenal Section, Department of Medicine, Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts; Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts.
Weining LuRenal Section, Department of Medicine, Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts; Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts. Electronic address: wlu@bu.edu.
Boston University · USPfizer (United States) · US

Funding

Molecular Pathogenesis of Vesicoureteral RefluxR01DK078226 · NIDDK · BOSTON MEDICAL CENTER · PI LU, WEINING · 2008 to 2018
$2.5M
Role of PLA2R and anti-PLA2R in idiopathic membranous nephropathyR01DK090029 · NIDDK · BOSTON MEDICAL CENTER · PI SALANT, DAVID J · 2011 to 2015
$1.9M
New Therapeutic Leads for Proteinuric Kidney DiseasesR01DK133940 · NIDDK · BOSTON MEDICAL CENTER · PI LU, WEINING · 2022 to 2024
$790k
NIDDK NIH HHS R01 DK078226NIDDK NIH HHS R01 DK090029NIDDK NIH HHS R01 DK133940
6 · The paper itself

Abstract

Roundabout guidance receptor 2 (ROBO2) plays an important role during early kidney development. ROBO2 is expressed in podocytes, inhibits nephrin-induced actin polymerization, down-regulates nonmuscle myosin IIA activity, and destabilizes kidney podocyte adhesion. However, the role of ROBO2 during kidney injury, particularly in mature podocytes, is not known. Herein, we report that loss of ROBO2 in podocytes [Robo2 conditional knockout (cKO) mouse] is protective from glomerular injuries. Ultrastructural analysis reveals that Robo2 cKO mice display less foot process effacement and better-preserved slit-diaphragm density compared with wild-type littermates injured by either protamine sulfate or nephrotoxic serum (NTS). The Robo2 cKO mice also develop less proteinuria after NTS injury. Further studies reveal that ROBO2 expression in podocytes is up-regulated after glomerular injury because its expression levels are higher in the glomeruli of NTS injured mice and passive Heymann membranous nephropathy rats. Moreover, the amount of ROBO2 in the glomeruli is also elevated in patients with membranous nephropathy. Finally, overexpression of ROBO2 in cultured mouse podocytes compromises cell adhesion. Taken together, these findings suggest that kidney injury increases glomerular ROBO2 expression that might compromise podocyte adhesion and, thus, loss of Robo2 in podocytes could protect from glomerular injury by enhancing podocyte adhesion that helps maintain foot process structure. Our findings also suggest that ROBO2 is a therapeutic target for podocyte injury and podocytopathy.

Indexed as

AdultAnimalsFemaleHumansKidney DiseasesKidney GlomerulusMaleMiceMice, Inbred C57BLPodocytesProtective AgentsProteinuriaRatsReceptors, ImmunologicRoundabout ProteinsProtective AgentsReceptors, ImmunologicROBO2 protein, humanRobo2 protein, mouseRobo2 protein, ratRoundabout Proteins

Identifiers

PMID32220420
PMCPMC7217334
OpenAlexW3013971876

What OpenQuestion holds

Textmetadata
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Registered trials

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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.