Evidence map›Paper›PMID 37870704›Full record

ReviewHeart failure reviews2024

The role of periostin in cardiac fibrosis.

Bao Qiao, Xuehao Liu, Bailu Wang, Shujian Wei

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2024. 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
4.0field-weighted citation impact, top 5% 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, 18 citations in OpenAlex.

  1. Article
  2. Identification and characterization of POSTNJournal of orthopaedic translation · 2026
    Article
  3. Article
  4. 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
    Article
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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

4 authors at 1 institution in 1 country.

Bao QiaoDepartment of Emergency and Chest Pain Center, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, China.
Xuehao LiuDepartment of Emergency and Chest Pain Center, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, China.
Bailu WangClinical Trial Center, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, China.
Shujian WeiDepartment of Emergency and Chest Pain Center, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, China. weishujian@sdu.edu.cn.ORCID 0000-0002-0896-6032
Qilu Hospital of Shandong University · CN

Funding

Clinical Research Foundation of Shandong University 2020SDUCRCC014National Natural Science Foundation of China 82072141National Natural Science Foundation of China 82202376Natural Science Foundation of Shandong Province ZR2020MH030Natural Science Foundation of Shandong Province ZR2022QH225
6 · The paper itself

Abstract

Cardiac fibrosis, which is the buildup of proteins in the connective tissues of the heart, can lead to end-stage extracellular matrix (ECM) remodeling and ultimately heart failure. Cardiac remodeling involves changes in gene expression in cardiac cells and ECM, which significantly leads to the morbidity and mortality in heart failure. However, despite extensive research, the elusive intricacies underlying cardiac fibrosis remain unidentified. Periostin, an extracellular matrix (ECM) protein of the fasciclin superfamily, acts as a scaffold for building complex architectures in the ECM, which improves intermolecular interactions and augments the mechanical properties of connective tissues. Recent research has shown that periostin not only contributes to normal ECM homeostasis in a healthy heart but also serves as a potent inducible regulator of cellular reorganization in cardiac fibrosis. Here, we reviewed the constitutive domain of periostin and its interaction with other ECM proteins. We have also discussed the critical pathophysiological functions of periostin in cardiac remodeling mechanisms, including two distinct yet potentially intertwined mechanisms. Furthermore, we will focus on the intrinsic complexities within periostin research, particularly surrounding the contentious issues observed in experimental findings.

Indexed as

Heart FailurePeriostinCell Adhesion MoleculesFibrosisHeartHumansVentricular RemodelingCell Adhesion MoleculesPeriostinPOSTN protein, humanAlternative splicingCardiac fibrosisCardiac remodelingECM proteinMechanical stressPeriostin

Identifiers

PMID37870704
OpenAlexW4387865920

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.