Evidence map›Paper›PMID 39818254›Full record

ArticleMatrix biology : journal of the International Society for Matrix Biology2025

Endothelial cell (EC)-specific Ctgf/Ccn2 expression increases EC reprogramming and atherosclerosis.

Feifei Li, Sandeep Kumar, Anastassia Pokutta-Paskaleva, Dong-Won Kang, Chanwoo Kim, Julia Raykin, Victor Omojola, Carson Hoffmann, Fujie Zhao, Maiko Teichmann and 12 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Matrix biology : journal of the International Society for Matrix Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. 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

22 authors.

Feifei LiDepartment of Surgery, Emory University, Atlanta, GA, USA.
Sandeep KumarWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Anastassia Pokutta-PaskalevaDepartment of Surgery, Emory University, Atlanta, GA, USA.
Dong-Won KangWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Chanwoo KimDepartment of Advanced Animal Model Development, Non-Clinical Center, Osong Medical Innovation Foundation (KBIO), Cheongju, Republic of Korea.
Julia RaykinDepartment of Surgery, Emory University, Atlanta, GA, USA.
Victor OmojolaWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Carson HoffmannDepartment of Surgery, Emory University, Atlanta, GA, USA; Research Services, Atlanta VA Medical Center, Decatur, GA, USA.
Fujie ZhaoDepartment of Surgery, Emory University, Atlanta, GA, USA; Research Services, Atlanta VA Medical Center, Decatur, GA, USA.
Maiko TeichmannDepartment of Surgery, Emory University, Atlanta, GA, USA; Research Services, Atlanta VA Medical Center, Decatur, GA, USA.
Christian ParkWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Kyung In BaekWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Gloriani Sanchez MarreroDepartment of Surgery, Emory University, Atlanta, GA, USA; Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Jing MaDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Hiromi YanagisawaLife Science Center, Tsukuba Advanced Research Alliance, University of Tsukuba, Tennodai 1-1-1, Tsukuba, Ibaraki 305-8577, Japan.
Andrew LeaskCollege of Dentistry, University of Saskatchewan, 105 Wiggins Rd, Saskatoon, SK, Canada.
Lucas TimminsDepartment of Bioengineering, University of Utah, Salt Lake City, UT, USA.
Xiangqin CuiDepartment of Biostatistics and Bioinformatics, Emory University, Atlanta, GA, USA.
Roy SutliffNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Rudy L GleasonWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA; George W. Woodruff School of Mechanical Engineering, Georgia Institute of Technology, Atlanta, GA, USA.
Hanjoong JoWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Luke P BrewsterDepartment of Surgery, Emory University, Atlanta, GA, USA; Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA; Research Services, Atlanta VA Medical Center, Decatur, GA, USA. Electronic address: lbrewst@emory.edu.

Funding

Molecular Mechanisms of Flow-dependent Arterial Remodeling in Peripheral Arterial DiseaseR01HL143348 · NHLBI · EMORY UNIVERSITY · PI BREWSTER, LUKE PACKARD · 2018 to 2022
$3.6M
NHLBI NIH HHS R01 HL143348
6 · The paper itself

Abstract

Arterial endothelial cells (ECs) reside in a complex biomechanical environment. ECs sense and respond to wall shear stress. Low and oscillatory wall shear stress is characteristic of disturbed flow and commonly found at arterial bifurcations and around atherosclerotic plaques. Disturbed flow is pro-inflammatory to ECs. Arteries also stiffen with aging and/or the onset of vascular disease. ECs sense and respond to stiffening in a pro-fibrotic manner. Thus, flow and stiffening disturbances elicit EC responses that promote pathologic arterial remodeling. However, the pathways elicited by ECs under pathologic stiffening and disturbed flow are not well understood. The objective of this work was to discover and test the modifiability of key pathways in ECs. To do this we used the partial carotid ligation model to impose disturbed flow onto the precociously stiffened fibulin-5 knockout (Fbln5

Indexed as

AtherosclerosisConnective Tissue Growth FactorEndothelial CellsAnimalsCarotid ArteriesDisease Models, AnimalExtracellular Matrix ProteinsFemaleHumansMaleMiceMice, KnockoutPlaque, AtheroscleroticCCN2 protein, humanCCN2 protein, mouseConnective Tissue Growth FactorExtracellular Matrix ProteinsArterial stiffeningAtherosclerotic plaqueConnective tissue growth factor/CCN2Endothelial cellsFibulin-5Flow-mediated arterial remodelingSex-differences

Identifiers

PMID39818254
PMCPMC11875889

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.