Evidence map›Paper›PMID 21854746›Full record

ArticleThe American journal of pathology2011

Periostin is induced in glomerular injury and expressed de novo in interstitial renal fibrosis.

Kontheari Sen, Maja T Lindenmeyer, Ariana Gaspert, Felix Eichinger, Matthias A Neusser, Matthias Kretzler, Stephan Segerer, Clemens D Cohen

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.9field-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

54 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Research progress of periostin and osteoporosis.Frontiers in endocrinology · 2024
    Review
  6. Article
  7. Article
  8. Periostin in Osteoporosis and Cardiovascular Disease.Journal of the Endocrine Society · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Periostin: biology and function in cancer.Cancer cell international · 2022
    Review
  13. Tissue mechanics coevolves with fibrillar matrisomes in healthy and fibrotic tissues.Matrix biology : journal of the International Society for Matrix Biology · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. The role of periostin in kidney diseases.Central-European journal of immunology · 2021
    Review
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

8 authors at 3 institutions in 2 countries.

Kontheari SenInstitute of Physiology and Division of Nephrology, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland.
Maja T Lindenmeyer
Ariana Gaspert
Felix Eichinger
Matthias A Neusser
Matthias Kretzler
Stephan Segerer
Clemens D Cohen
University of Zurich · CHUniversity Hospital of Zurich · CHUniversity of Michigan · US

Funding

University of Michigan O'Brien Kidney Translational Core CenterP30DK081943 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PENNATHUR, SUBRAMANIAM · 2008 to 2022
$12.9M
NIDDK NIH HHS P30 DK081943NIDDK NIH HHS P30DK081943-01
6 · The paper itself

Abstract

Matricellular proteins participate in the pathogenesis of chronic kidney diseases. We analyzed glomerular gene expression profiles from patients with proteinuric diseases to identify matricellular proteins contributing to the progression of human nephropathies. Several genes encoding matricellular proteins, such as SPARC, THBS1, and CTGF, were induced in progressive nephropathies, but not in nonprogressive minimal-change disease. Periostin showed the highest induction, and its transcript levels correlated negatively with glomerular filtration rate in both glomerular and tubulointerstitial specimen. In well-preserved renal tissue, periostin localized to the glomerular tuft, the vascular pole, and along Bowman's capsule; no signal was detected in the tubulointerstitial compartment. Biopsies from patients with glomerulopathies and renal dysfunction showed enhanced periostin expression in the mesangium, tubular interstitium, and sites of fibrosis. Periostin staining correlated negatively with renal function. α-smooth muscle actin-positive mesangial and interstitial cells localized close to periostin-positive sites, as indicated by co-immunofluorescence. In vitro stimulation of mesangial cells by external addition of TGF-β1 resulted in robust induction of periostin. Addition of periostin to mesangial cells induced cell proliferation and decreased the number of cells expressing activated caspase-3, a marker of apoptosis. These human data indicate for the first time a role of periostin in glomerular and interstitial injury in acquired nephropathies.

Indexed as

AdolescentAdultAgedAged, 80 and overApoptosisBiopsyCell Adhesion MoleculesCell ProliferationFemaleFibrosisHumansImmunohistochemistryKidney Failure, ChronicKidney GlomerulusMaleMesangial CellsCell Adhesion MoleculesPOSTN protein, human

Identifiers

PMID21854746
PMCPMC3181392
OpenAlexW1974167931

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.