Evidence map›Paper›PMID 35470068›Full record

ArticleMatrix biology : journal of the International Society for Matrix Biology2022

Asporin, an extracellular matrix protein, is a beneficial regulator of cardiac remodeling.

Chengqun Huang, Ankush Sharma, Reetu Thakur, Deepika Rai, Madhusudhanarao Katiki, Juliana de Freitas Germano, Yang Song, Sakshi Singh, Jon Sin, David Sengstock and 5 more

Open access · greenAbstract read
In one paragraph

Article in Matrix biology : journal of the International Society for Matrix Biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

31 citing papers in PubMed, 42 citations in OpenAlex.

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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

15 authors at 5 institutions in 2 countries.

Chengqun HuangDepartment of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA USA.
Ankush SharmaDepartment of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, 0310 Oslo, Norway; KG Jebsen Centre for B-Cell Malignancies, Institute for Clinical Medicine, University of Oslo, 0318 Oslo, Norway.
Reetu ThakurDepartment of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA USA.
Deepika RaiDepartment of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA USA.
Madhusudhanarao KatikiDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California USA.
Juliana de Freitas GermanoDepartment of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA USA.
Yang SongDepartment of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA USA.
Sakshi SinghDivision of Biochemistry, Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway; Centre for Cancer Cell Reprogramming, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Jon SinDepartment of Biological Sciences, The University of Alabama Tuscaloosa, Alabama.
David SengstockDepartment of Internal Medicine, Beaumont Hospital and Wayne State University, Dearborn, Michigan, USA.
Allen M AndresDepartment of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA USA.
Ramachandran MuraliDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California USA.
Robert M MentzerDepartment of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA USA.
Roberta A GottliebDepartment of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA USA; Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California USA.
Honit PiplaniDepartment of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA USA; Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California USA. Electronic address: honit.piplani@cshs.org.
Cedars-Sinai Medical Center · USOslo University Hospital · NOUniversity of Alabama · USUniversity of Oslo · NOWayne State University · US

Funding

Regulation of the Dynamic Proteome after Ischemic InjuryR01HL144509 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI GOTTLIEB, ROBERTA A., VAN EYK, JENNIFER E · 2019 to 2022
$2.9M
Asporin, an extracellular protein, regulates cardiac remodelingR01HL155553 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI PARKER, SARAH J · 2021 to 2025
$2.1M
NHLBI NIH HHS R01 HL144509NHLBI NIH HHS R01 HL155553
6 · The paper itself

Abstract

Heart failure is accompanied by adverse cardiac remodeling involving extracellular matrix (ECM). Cardiac ECM acts as a major reservoir for many proteins including growth factors, cytokines, collagens, and proteoglycans. Activated fibroblasts during cardiac injury can alter the composition and activity of these ECM proteins. Through unbiased analysis of a microarray dataset of human heart tissue comparing normal hearts (n = 135) to hearts with ischemic cardiomyopathy (n = 94), we identified Asporin (ASPN) as the top differentially regulated gene (DEG) in ischemic cardiomyopathy; its gene-ontology terms relate closely to fibrosis and cell death. ASPN is a Class I small leucine repeat protein member implicated in cancer, osteoarthritis, and periodontal ligament mineralization. However, its role in cardiac remodeling is still unknown. Here, we initially confirmed our big dataset analysis through cells, mice, and clinical atrial biopsy samples to demonstrate increased Aspn expression after pressure overload or cardiac ischemia/reperfusion injury. We tested the hypothesis that Aspn, being a TGFβ1 inhibitor, can attenuate fibrosis in mouse models of cardiac injury. We found that Aspn is released by cardiac fibroblasts and attenuates TGFβ signaling. Moreover, Aspn

Indexed as

CardiomyopathiesHeart FailureReperfusion InjuryAnimalsDisease Models, AnimalExtracellular MatrixExtracellular Matrix ProteinsFibrosisInfarctionIschemiaMiceMice, Inbred C57BLMyocytes, CardiacVentricular RemodelingExtracellular Matrix ProteinsAsporinCardiac remodelingECMFibrosisIschemia

Identifiers

PMID35470068
PMCPMC10234622
OpenAlexW4224269882

What OpenQuestion holds

Textmetadata
LicenceTDM
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.