Evidence map›Paper›PMID 34196216›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2021

Endothelial-Mesenchymal Transition in Cardiovascular Disease.

Zahra Alvandi, Joyce Bischoff

Open access · bronzeAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed
9.5field-weighted citation impact, top 1% 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

144 citing papers in PubMed, 192 citations in OpenAlex.

  1. Review
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84 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Zahra AlvandiVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, MA.
Joyce BischoffVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, MA.
Boston Children's Hospital · US

Funding

PROGRAM IN BLOOD COAGULATION AND VASCULAR BIOLOGYT32HL007917 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Robert C Flaumenhaft · 1999 to 2026
$11.1M
Improving Mitral Compensation In Ischemic RegurgitationR01HL141917 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI AIKAWA, ELENA, BISCHOFF, JOYCE E. · 2018 to 2021
$5.6M
CD45-mediated endothelial-to-mesenchymal transition in cardiovascular diseaseR01HL141853 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, WANG, DA-ZHI · 2020 to 2023
$3.3M
Molecular Mechanisms Regulating Endothelial DysfunctionR01HL137229 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, SRIVASTAVA, SANJAY · 2017 to 2020
$2.7M
NHLBI NIH HHS R01 HL137229NHLBI NIH HHS R01 HL141853NHLBI NIH HHS R01 HL141917NHLBI NIH HHS T32 HL007917
6 · The paper itself

Abstract

Endothelial-to-mesenchymal transition is a dynamic process in which endothelial cells suppress constituent endothelial properties and take on mesenchymal cell behaviors. To begin the process, endothelial cells loosen their cell-cell junctions, degrade the basement membrane, and migrate out into the perivascular surroundings. These initial endothelial behaviors reflect a transient modulation of cellular phenotype, that is, a phenotypic modulation, that is sometimes referred to as partial endothelial-to-mesenchymal transition. Loosening of endothelial junctions and migration are also seen in inflammatory and angiogenic settings such that endothelial cells initiating endothelial-to-mesenchymal transition have overlapping behaviors and gene expression with endothelial cells responding to inflammatory signals or sprouting to form new blood vessels. Reduced endothelial junctions increase permeability, which facilitates leukocyte trafficking, whereas endothelial migration precedes angiogenic sprouting and neovascularization; both endothelial barriers and quiescence are restored as inflammatory and angiogenic stimuli subside. Complete endothelial-to-mesenchymal transition proceeds beyond phenotypic modulation such that mesenchymal characteristics become prominent and endothelial functions diminish. In proadaptive, regenerative settings the new mesenchymal cells produce extracellular matrix and contribute to tissue integrity whereas in maladaptive, pathologic settings the new mesenchymal cells become fibrotic, overproducing matrix to cause tissue stiffness, which eventually impacts function. Here we will review what is known about how TGF (transforming growth factor) β influences this continuum from junctional loosening to cellular migration and its relevance to cardiovascular diseases.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsCardiovascular DiseasesCell MovementEndothelial CellsEndothelium, VascularHumansPermeabilityPhenotypeSignal Transductioncardiovascular diseaseendothelial cellsmitral valve insufficiencyphenotypetransforming growth factor

Identifiers

PMID34196216
PMCPMC8387428
OpenAlexW3176328315

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.