Evidence map›Paper›PMID 31690575›Full record

ArticleJournal of the American Society of Nephrology : JASN2020

Periostin Promotes Cell Proliferation and Macrophage Polarization to Drive Repair after AKI.

Raphaёl Kormann, Panagiotis Kavvadas, Sandrine Placier, Sophie Vandermeersch, Aude Dorison, Jean-Claude Dussaule, Christos E Chadjichristos, Niki Prakoura, Christos Chatziantoniou

Open access · greenAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

55 citing papers in PubMed, 87 citations in OpenAlex.

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  15. Effect of periostin (OSF-2) on phagocytosis ofFrontiers in microbiology · 2025
    Article
  16. Article
  17. Article
  18. Cell-cell communication in kidney fibrosis.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024
    Review
  19. Rodent models of AKI and AKI-CKD transition: an update in 2024.American journal of physiology. Renal physiology · 2024
    Review
  20. 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

9 authors at 3 institutions in 1 country.

Raphaёl KormannInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche Scientifique 1155, Tenon Hospital, Paris, France; and.
Panagiotis KavvadasInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche Scientifique 1155, Tenon Hospital, Paris, France; and.
Sandrine PlacierInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche Scientifique 1155, Tenon Hospital, Paris, France; and.
Sophie VandermeerschInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche Scientifique 1155, Tenon Hospital, Paris, France; and.
Aude DorisonInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche Scientifique 1155, Tenon Hospital, Paris, France; and.
Jean-Claude DussauleInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche Scientifique 1155, Tenon Hospital, Paris, France; and.
Christos E ChadjichristosInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche Scientifique 1155, Tenon Hospital, Paris, France; and.
Niki PrakouraInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche Scientifique 1155, Tenon Hospital, Paris, France; and.
Christos ChatziantoniouInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche Scientifique 1155, Tenon Hospital, Paris, France; and christos.chatziantoniou@upmc.fr.
Sorbonne Université · FRHôpital Tenon · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe matricellular protein periostin has been associated with CKD progression in animal models and human biopsy specimens. Periostin functions by interacting with extracellular matrix components to drive collagen fibrillogenesis and remodeling or by signaling through cell-surface integrin receptors to promote cell adhesion, migration, and proliferation. However, its role in AKI is unknown.

methodsWe used mice with conditional tubule-specific overexpression of periostin or knockout mice lacking periostin expression in the renal ischemia-reperfusion injury model, and primary cultures of isolated tubular cells in a hypoxia-reoxygenation model.

resultsTubular epithelial cells showed strong production of periostin during the repair phase of ischemia reperfusion. Periostin overexpression protected mice from renal injury compared with controls, whereas knockout mice showed increased tubular injury and deteriorated renal function. Periostin interacted with its receptor, integrin-

conclusionsIn contrast to the detrimental role of periostin in CKD, we discovered a protective role of periostin in AKI. Our findings suggest periostin may be a novel and important mediator of mechanisms controlling renal repair after AKI.

Indexed as

Acute Kidney InjuryCell ProliferationAnimalsCell Adhesion MoleculesDisease Models, AnimalKidneyMacrophagesMaleMiceMice, KnockoutReperfusion InjuryCell Adhesion MoleculesPostn protein, mouseacute renal failureapoptosiscell survivalischemia-reperfusionmacrophagestubular epithelium

Identifiers

PMID31690575
PMCPMC6935011
OpenAlexW2988910790

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.