Evidence map›Paper›PMID 28884334›Full record

ReviewCellular and molecular life sciences : CMLS2017

Periostin in kidney diseases.

Niki Prakoura, Christos Chatziantoniou

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Role of local complement activation in kidney fibrosis and repair.The Journal of clinical investigation · 2025
    Review
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  19. NRF2 Activation Inhibits Both TGF-Oxidative medicine and cellular longevity · 2018
    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

2 authors at 1 institution in 1 country.

Niki PrakouraInstitut National de la Santé Et de la Recherche Médicale UMRS 1155, Tenon Hospital, 4 rue de la Chine, 75020, Paris, France. niki.prakoura@gmail.com.
Christos ChatziantoniouInstitut National de la Santé Et de la Recherche Médicale UMRS 1155, Tenon Hospital, 4 rue de la Chine, 75020, Paris, France.
Sorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease is an incurable to date pathology, with renal replacement therapy through dialysis or transplantation being the only available option for end-stage patients. A deeper understanding of the molecular mechanisms governing the progression of kidney diseases will permit the identification of unknown mediators and potential novel markers or targets of therapy which promise more efficient diagnostic and therapeutic applications. Over the last years, periostin was established by several studies as a novel key player in the progression of renal disease. Periostin is de novo expressed focally by the injured kidney cells during the development of renal disease. In diverse cohorts of renal disease patients, the expression levels of periostin in the kidney and urine were highly correlated with the stage of the pathology and the decline of renal function. Subsequent studies in animal models demonstrated that periostin is centrally involved in mediating renal inflammation and fibrosis, contributing to the deterioration of renal structure and function. Genetic or pharmaco-genetic inhibition of periostin in animal models of renal disease was efficient in arresting the progression of the pathology. This review will summarize the recent advances on periostin in the field of kidney diseases and will discuss its utility of as a novel target of therapy for chronic kidney disease.

Indexed as

AnimalsAntibodies, MonoclonalCell Adhesion MoleculesCollagen Type ICytokinesDisease Models, AnimalDisease ProgressionFibrosisGene Expression RegulationHumansKidneyMolecular Targeted TherapyRenal Insufficiency, ChronicRNA, Small InterferingSignal TransductionAntibodies, MonoclonalCell Adhesion MoleculesCollagen Type ICytokinesPOSTN protein, humanRNA, Small InterferingChronic kidney diseaseFibrosisInflammationPeriostinTarget of therapy

Identifiers

PMID28884334
PMCPMC11107687
OpenAlexW2752347781

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.