Evidence map›Paper›PMID 36529756›Full record

ArticleScientific reports2022

Defining the timeline of periostin upregulation in cardiac fibrosis following acute myocardial infarction in mice.

Hadas Gil, Matan Goldshtein, Sharon Etzion, Sigal Elyagon, Uzi Hadad, Yoram Etzion, Smadar Cohen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Differential transcriptomic and metabolomic landscape between human hearts donated after cardiac vs brain death.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2026
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  10. Review
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  15. Article
  16. Proteomics Reveals Increased Periostin in Synovial Fluid From Canine and Human Anterior Cruciate Ligament Injury.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025
    Article
  17. Article
  18. Periostin in Bronchiolitis Obliterans Syndrome after Lung Transplant.International journal of molecular sciences · 2024
    Article
  19. Article
  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

7 authors at 1 institution in 1 country.

Hadas GilAvram and Stella Goldstein-Goren Department of Biotechnology Engineering, Ben-Gurion University of the Negev, POB 653, 8410501, Beer-Sheva, Israel.
Matan GoldshteinAvram and Stella Goldstein-Goren Department of Biotechnology Engineering, Ben-Gurion University of the Negev, POB 653, 8410501, Beer-Sheva, Israel.
Sharon EtzionRegenerative Medicine and Stem Cell (RMSC) Research Center, Ben-Gurion University of the Negev, 8410501, Beer-Sheva, Israel.
Sigal ElyagonDepartment of Physiology and Cell Biology, Ben-Gurion University of the Negev, 8410501, Beer-Sheva, Israel.
Uzi HadadThe Ilse Katz Institute for Nanoscale Science and Technology, Ben-Gurion University of the Negev, 8410501, Beer-Sheva, Israel.
Yoram EtzionRegenerative Medicine and Stem Cell (RMSC) Research Center, Ben-Gurion University of the Negev, 8410501, Beer-Sheva, Israel.
Smadar CohenAvram and Stella Goldstein-Goren Department of Biotechnology Engineering, Ben-Gurion University of the Negev, POB 653, 8410501, Beer-Sheva, Israel. scohen@bgu.ac.il.
Ben-Gurion University of the Negev · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

After myocardial infarction (MI), the heart's reparative response to the ischemic insult and the related loss of cardiomyocytes involves cardiac fibrosis, in which the damaged tissue is replaced with a fibrous scar. Although the scar is essential to prevent ventricular wall rupture in the infarction zone, it expands over time to remote, non-infarct areas, significantly increasing the extent of fibrosis and markedly altering cardiac structure. Cardiac function in this scenario deteriorates, thereby increasing the probability of heart failure and the risk of death. Recent works have suggested that the matricellular protein periostin, known to be involved in fibrosis, is a candidate therapeutic target for the regulation of MI-induced fibrosis and remodeling. Different strategies for the genetic manipulation of periostin have been proposed previously, yet those works did not properly address the time dependency between periostin activity and cardiac fibrosis. Our study aimed to fill that gap in knowledge and fully elucidate the explicit timing of cellular periostin upregulation in the infarcted heart to enable the safer and more effective post-MI targeting of periostin-producing cells. Surgical MI was performed in C57BL/6J and BALB/c mice by ligation of the left anterior descending coronary artery. Flow cytometry analyses of cells derived from the infarcted hearts and quantitative real-time PCR of the total cellular RNA revealed that periostin expression increased during days 2-7 and peaked on day 7 post-infarct, regardless of mouse strain. The established timeline for cellular periostin expression in the post-MI heart is a significant milestone toward the development of optimal periostin-targeted gene therapy.

Indexed as

CicatrixMyocardial InfarctionAnimalsCell Adhesion MoleculesDisease Models, AnimalFibrosisMiceMice, Inbred C57BLMyocardiumMyocytes, CardiacUp-RegulationVentricular RemodelingCell Adhesion MoleculesPostn protein, mouse

Identifiers

PMID36529756
PMCPMC9760637
OpenAlexW4312066246

What OpenQuestion holds

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Registered trials

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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.