Evidence map›Paper›PMID 28928136›Full record

ArticleJournal of the American Society of Nephrology : JASN2017

Endothelial

Yosu Luque, Olivia Lenoir, Philippe Bonnin, Lise Hardy, Anna Chipont, Sandrine Placier, Sophie Vandermeersch, Yi-Chun Xu-Dubois, Blaise Robin, Hélène Lazareth and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

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  17. Glomerular disease: Loss of Epas1 promotes FSGS.Nature reviews. Nephrology · 2017
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 9 institutions in 2 countries.

Yosu LuqueCritical Care Nephrology and Kidney Transplantation, Hôpital Tenon, Assistance Publique-Hôpitaux de Paris, Paris, France.
Olivia LenoirParis Cardiovascular Center (PARCC).
Philippe BonninDepartment of Physiology, Hôpital Lariboisière, Assistance Publique-Hôpitaux de Paris, Paris, France.
Lise HardyUnité Mixte de Recherche S1155.
Anna ChipontParis Cardiovascular Center (PARCC).
Sandrine PlacierUnité Mixte de Recherche S1155.
Sophie VandermeerschUnité Mixte de Recherche S1155.
Yi-Chun Xu-DuboisCritical Care Nephrology and Kidney Transplantation, Hôpital Tenon, Assistance Publique-Hôpitaux de Paris, Paris, France.
Blaise RobinParis Cardiovascular Center (PARCC).
Hélène LazarethParis Cardiovascular Center (PARCC).
Michèle SouyriInstitut Universitaire d'Hématologie, Institut National de la Santé et de la Recherche Médicale, Paris, France.
Léa GuyonnetNational Cytometry Platform, Department of Infection and Immunity, Luxembourg Institute of Health, Esch-sur-Alzette, Luxembourg; and.
Véronique BaudrieParis Cardiovascular Center (PARCC).
Eric CamererParis Cardiovascular Center (PARCC).
Eric RondeauCritical Care Nephrology and Kidney Transplantation, Hôpital Tenon, Assistance Publique-Hôpitaux de Paris, Paris, France.
Laurent MesnardCritical Care Nephrology and Kidney Transplantation, Hôpital Tenon, Assistance Publique-Hôpitaux de Paris, Paris, France.
Pierre-Louis TharauxParis Cardiovascular Center (PARCC), pierre-louis.tharaux@inserm.fr.
Assistance Publique – Hôpitaux de Paris · FRParis Cardiovascular Research Center · FRSorbonne Paris Cité · FRDélégation Paris 5 · FRHôpital Tenon · FRInstitut Universitaire de France · FRLuxembourg Institute of Health · LUSorbonne Université · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FSGS, the most common primary glomerular disorder causing ESRD, is a complex disease that is only partially understood. Progressive sclerosis is a hallmark of FSGS, and genetic tracing studies have shown that parietal epithelial cells participate in the formation of sclerotic lesions. The loss of podocytes triggers a focal activation of parietal epithelial cells, which subsequently form cellular adhesions with the capillary tuft. However, in the absence of intrinsic podocyte alterations, the origin of the pathogenic signal that triggers parietal epithelial cell recruitment remains elusive. In this study, investigation of the role of the endothelial PAS domain-containing protein 1 (EPAS1), a regulatory

Indexed as

Gene Expression RegulationAlbuminsAngiotensin IIAnimalsBasic Helix-Loop-Helix ProteinsBlood PressureCell DifferentiationCrosses, GeneticDisease ProgressionEndothelial PAS Domain-Containing Protein 1Epithelial CellsGene DeletionGlomerulosclerosis, Focal SegmentalHypertensionKidney GlomerulusMaleAlbuminsAngiotensin IIBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1endothelial cellsfocal segmental glomerulosclerosisglomerular endothelial cellsglomerular epithelial cellshypertensionPathophysiology of Renal Disease and Progression

Identifiers

PMID28928136
PMCPMC5698059
OpenAlexW2754666939

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.