Evidence map›Paper›PMID 31816901›Full record

ReviewCells2019

Osteopontin: A Promising Therapeutic Target in Cardiac Fibrosis.

Iman Abdelaziz Mohamed, Alain-Pierre Gadeau, Anwarul Hasan, Nabeel Abdulrahman, Fatima Mraiche

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.2field-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

53 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Pulmonary fibrosis: Emerging targets and novel therapeutics.The Journal of international medical research · 2026
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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

5 authors at 4 institutions in 3 countries.

Iman Abdelaziz MohamedVisiting Scholar, Center of Excellence for Stem Cells and Regenerative Medicine (CESC), Zewail City of Science and Technology, 6th of October City, P.O. Box 12588 Giza Governorate, Egypt.ORCID 0000-0002-9207-823X
Alain-Pierre GadeauINSERM, Biology of Cardiovascular Disease, University of Bordeaux, U1034 Pessac, France.ORCID 0000-0003-1312-6481
Anwarul HasanDepartment of Mechanical and Industrial Engineering, College of Engineering, Qatar University, P.O. Box 2713 Doha, Qatar.
Nabeel AbdulrahmanTranslational Research Institute, Academic Health System, Hamad Medical Corporation, P.O. Box 3050 Doha, Qatar.
Fatima MraicheDepartment of Pharmaceutical Sciences, College of Pharmacy, QU Health, Qatar University, P.O. Box 2713 Doha, Qatar.ORCID 0000-0001-6188-1145
Qatar University · QAHamad Medical Corporation · QAUniversité de Bordeaux · FRZewail City of Science and Technology · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteopontin (OPN) is recognized for its significant roles in both physiological and pathological processes. Initially, OPN was recognized as a cytokine with pro-inflammatory actions. More recently, OPN has emerged as a matricellular protein of the extracellular matrix (ECM). OPN is also known to be a substrate for proteolytic cleavage by several proteases that form an integral part of the ECM. In the adult heart under physiological conditions, basal levels of OPN are expressed. Increased expression of OPN has been correlated with the progression of cardiac remodeling and fibrosis to heart failure and the severity of the condition. The intricate process by which OPN mediates its effects include the coordination of intracellular signals necessary for the differentiation of fibroblasts into myofibroblasts, promoting angiogenesis, wound healing, and tissue regeneration. In this review, we discuss the role of OPN in contributing to the development of cardiac fibrosis and its suitability as a therapeutic target.

Indexed as

BiomarkersCardiomyopathiesDisease SusceptibilityFibrosisGene Expression RegulationHeart DiseasesHumansOsteopontinSignal TransductionBiomarkersOsteopontinbiomarkercardiac fibrosisinflammationosteopontinpotential therapeutic target

Identifiers

PMID31816901
PMCPMC6952988
OpenAlexW2992878053

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.