Evidence map›Paper›PMID 24937434›Full record

ReviewBiochimica et biophysica acta2015

Epigenetic regulation of smooth muscle cell plasticity.

Renjing Liu, Kristen L Leslie, Kathleen A Martin

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
6.4field-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

78 citing papers in PubMed, 136 citations in OpenAlex.

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  17. Pro-Healing Nanomatrix-Coated Stent Analysis in anACS applied materials & interfaces · 2022
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  19. Review
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18 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

3 authors at 2 institutions in 2 countries.

Renjing LiuAgnes Ginges Laboratory for Diseases of the Aorta, Centre for the Endothelium, Vascular Biology Program, Centenary Institute, Sydney, Australia; Sydney Medical School, University of Sydney, Australia.
Kristen L LeslieDepartments of Internal Medicine and Pharmacology, Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Yale University, New Haven, CT 06511, USA.
Kathleen A MartinDepartments of Internal Medicine and Pharmacology, Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Yale University, New Haven, CT 06511, USA. Electronic address: kathleen.martin@yale.edu.
Yale University · USUniversity of Sydney · AU

Funding

Novel targets of rapamycin and Akt in vascular smooth muscle cell differentiationR01HL091013 · NHLBI · YALE UNIVERSITY · PI MARTIN, KATHLEEN ANN · 2008 to 2017
$4.1M
Regulation of vascular smooth muscle cell plasticityR01HL118430 · NHLBI · YALE UNIVERSITY · PI MARTIN, KATHLEEN ANN · 2014 to 2017
$1.7M
Epigenetic control of vascular smooth muscle in cardiovascular diseaseR01HL119529 · NHLBI · YALE UNIVERSITY · PI MARTIN, KATHLEEN ANN · 2014 to 2017
$1.7M
NHLBI NIH HHS 1R01HL118430-01NHLBI NIH HHS R01 HL091013NHLBI NIH HHS R01HL091013ANHLBI NIH HHS R01 HL118430NHLBI NIH HHS R01 HL119529
6 · The paper itself

Abstract

Smooth muscle cells (SMC) are the major cell type in blood vessels. Their principal function in the body is to regulate blood flow and pressure through vessel wall contraction and relaxation. Unlike many other mature cell types in the adult body, SMC do not terminally differentiate but retain a remarkable plasticity. They have the unique ability to toggle between a differentiated and quiescent "contractile" state and a highly proliferative and migratory "synthetic" phenotype in response to environmental stresses. While there have been major advances in our understanding of SMC plasticity through the identification of growth factors and signals that can influence the SMC phenotype, how these regulate SMC plasticity remains unknown. To date, several key transcription factors and regulatory cis elements have been identified that play a role in modulating SMC state. The frontier in understanding the molecular mechanisms underlying SMC plasticity has now advanced to the level of epigenetics. This review will summarize the epigenetic regulation of SMC, highlighting the role of histone modification, DNA methylation, and our most recent identification of a DNA demethylation pathway in SMC that is pivotal in the regulation of the SMC phenotypic state. Many disorders are associated with smooth muscle dysfunction, including atherosclerosis, the major underlying cause of stroke and coronary heart disease, as well as transplant vasculopathy, aneurysm, asthma, hypertension, and cancer. An increased understanding of the major regulators of SMC plasticity will lead to the identification of novel target molecules that may, in turn, lead to novel drug discoveries for the treatment of these diseases. This article is part of a Special Issue entitled: Stress as a fundamental theme in cell plasticity.

Indexed as

AdultAnimalsCell DedifferentiationCell DifferentiationDioxygenasesDiseaseDNA-Binding ProteinsDNA MethylationEpigenesis, GeneticHealthHumansMyocytes, Smooth MuscleProto-Oncogene ProteinsDioxygenasesDNA-Binding ProteinsProto-Oncogene ProteinsTET2 protein, humanChromatinDNA methylationEpigeneticsSmooth muscle phenotypeTET2Transcription

Identifiers

PMID24937434
PMCPMC4552189
OpenAlexW2002233327

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.