Evidence map›Paper›PMID 36940798›Full record

ArticleKidney international2023

Podocyte protease activated receptor 1 stimulation in mice produces focal segmental glomerulosclerosis mirroring human disease signaling events.

Carl J May, Musleeha Chesor, Sarah E Hunter, Bryony Hayes, Rachel Barr, Tim Roberts, Fern A Barrington, Louise Farmer, Lan Ni, Maisie Jackson and 10 more

Open access · hybridAbstract read
In one paragraph

Article in Kidney international, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Serine proteases and protease-activated receptors signaling in the kidney.American journal of physiology. Cell physiology · 2025
    Review
  8. Article
  9. Effects of Prothrombin on Podocytopathy and Proteinuria in Glomerular Disease.Journal of the American Society of Nephrology : JASN · 2025
    Article
  10. Gene therapy and kidney diseases.Molecular therapy. Methods & clinical development · 2024
    Review
  11. Article
  12. Article
  13. Calcium signalling and transport in the kidney.Nature reviews. Nephrology · 2024
    Review
  14. Management of adult patients with podocytopathies: an update from the ERA Immunonephrology Working Group.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024
    Article
  15. Article
  16. What is circulating factor disease and how is it currently explained?Pediatric nephrology (Berlin, Germany) · 2023
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 5 institutions in 1 country.

Carl J MayBristol Renal, University of Bristol, Bristol, UK.
Musleeha ChesorBristol Renal, University of Bristol, Bristol, UK.
Sarah E HunterBristol Renal, University of Bristol, Bristol, UK.
Bryony HayesBristol Renal, University of Bristol, Bristol, UK.
Rachel BarrBristol Renal, University of Bristol, Bristol, UK.
Tim RobertsBristol Renal, University of Bristol, Bristol, UK.
Fern A BarringtonBristol Renal, University of Bristol, Bristol, UK.
Louise FarmerBristol Renal, University of Bristol, Bristol, UK.
Lan NiBristol Renal, University of Bristol, Bristol, UK.
Maisie JacksonBristol Renal, University of Bristol, Bristol, UK.
Heidi SnethenBristol Renal, University of Bristol, Bristol, UK.
Nadia TavakolidakhrabadiBristol Renal, University of Bristol, Bristol, UK.
Max GoldstoneBristol Renal, University of Bristol, Bristol, UK.
Rodney GilbertRenal Medicine and Nephrology, Southampton General Hospital, University Hospital Southampton, Southampton, UK.
Matt BeesleyPathology Department, Gloucestershire Royal Hospital, Gloucester, UK.
Rachel LennonWellcome Trust Centre for Cell Matrix Research, Division of Cell Matrix Biology and Regenerative Medicine, Faculty of Biology, Medical and Health Sciences, School of Biological Sciences, University of Manchester, Manchester, UK.
Rebecca FosterBristol Renal, University of Bristol, Bristol, UK.
Richard CowardBristol Renal, University of Bristol, Bristol, UK; Department of Paediatric Nephrology, Bristol Royal Hospital for Children, Bristol, UK.
Gavin I WelshBristol Renal, University of Bristol, Bristol, UK.
Moin A SaleemBristol Renal, University of Bristol, Bristol, UK; Department of Paediatric Nephrology, Bristol Royal Hospital for Children, Bristol, UK. Electronic address: m.saleem@bristol.ac.uk.
University of Bristol · GBBristol Royal Hospital for Children · GBGloucestershire Royal Hospital · GBUniversity Hospital Southampton NHS Foundation Trust · GBWellcome Centre for Cell-Matrix Research · GB

Funding

Medical Research Council G0501901Medical Research Council G0800200Medical Research Council MR/K010492/1Medical Research Council MR/L002418/1Medical Research Council MR/R003017/1Medical Research Council MR/T002263/1Medical Research Council MR/W019582/1
6 · The paper itself

Abstract

About 30% of patients who have a kidney transplant with underlying nephrotic syndrome (NS) experience rapid relapse of disease in their new graft. This is speculated to be due to a host-derived circulating factor acting on podocytes, the target cells in the kidney, leading to focal segmental glomerulosclerosis (FSGS). Our previous work suggests that podocyte membrane protease receptor 1 (PAR-1) is activated by a circulating factor in relapsing FSGS. Here, the role of PAR-1 was studied in human podocytes in vitro, and using a mouse model with developmental or inducible expression of podocyte-specific constitutively active PAR-1, and using biopsies from patients with nephrotic syndrome. In vitro podocyte PAR-1 activation caused a pro-migratory phenotype with phosphorylation of the kinase JNK, VASP protein and docking protein Paxillin. This signaling was mirrored in podocytes exposed to patient relapse-derived NS plasma and in patient disease biopsies. Both developmental and inducible activation of transgenic PAR-1 (NPHS2 Cre PAR-1

Indexed as

Glomerulosclerosis, Focal SegmentalNephrotic SyndromePodocytesAnimalsDisease Models, AnimalHumansReceptor, PAR-1RecurrenceTRPC6 Cation ChannelReceptor, PAR-1TRPC6 Cation Channelcirculating factornephrotic syndromePAR-1podocyteproteases

Identifiers

PMID36940798
PMCPMC7616342
OpenAlexW4327921304

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.