Evidence map›Paper›PMID 30184544›Full record

ReviewCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2018

Signaling Mechanisms of Myofibroblastic Activation: Outside-in and Inside-Out.

Joshua Zent, Lian-Wang Guo

Open access · goldAbstract readReview
In one paragraph

Review in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

70 citing papers in PubMed, 114 citations in OpenAlex.

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10 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 2 institutions in 1 country.

Joshua ZentMedical Scientist Training Program, the Ohio State University, Columbus, Columbus, Ohio, USA.
Lian-Wang GuoDepartment of Surgery, Department of Physiology & Cell Biology, College of Medicine, Davis Heart and Lung Research Institute, Wexner Medical Center, the Ohio State University, Columbus, Ohio, USA.
The Ohio State University · USThe Ohio State University Wexner Medical Center · US

Funding

Development of unimolecular nanoparticle-mediated periadventitial drug delivery system for sustained and targeted inhibition of intimal hyperplasia following open vascular reconstructionR01HL129785 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI GONG, SHAOQIN -, GUO, LIANWANG · 2016 to 2019
$2.0M
Sigma-1 Chaperone-Mediated in vivo Neuroprotection in the RetinaR01EY022678 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI GUO, LIANWANG · 2012 to 2016
$1.7M
BET Bromodomain proteins as Novel Epigenetic Targets for prevention of Intimal Hyperplasia after Vascular SurgeryR01HL133665 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI GUO, LIANWANG · 2016 to 2019
$1.6M
NEI NIH HHS R01 EY022678NHLBI NIH HHS R01 HL129785NHLBI NIH HHS R01 HL133665
6 · The paper itself

Abstract

Myofibroblasts are central mediators of fibrosis. Typically derived from resident fibroblasts, myofibroblasts represent a heterogeneous population of cells that are principally defined by acquired contractile function and high synthetic ability to produce extracellular matrix (ECM). Current literature sheds new light on the critical role of ECM signaling coupled with mechanotransduction in driving myofibroblastic activation. In particular, transforming growth factor β1 (TGF-β1) and extra domain A containing fibronectin (EDA-FN) are thought to be the primary ECM signaling mediators that form and also induce positive feedback loops. The outside-in and inside-out signaling circuits are transmitted and integrated by TGF-β receptors and integrins at the cell membrane, ultimately perpetuating the abundance and activities of TGF-β1 and EDA-FN in the ECM. In this review, we highlight these conceptual advances in understanding myofibroblastic activation, in hope of revealing its therapeutic anti-fibrotic implications.

Indexed as

Extracellular MatrixFibronectinsFocal AdhesionsHumansIntegrinsMechanotransduction, CellularMyofibroblastsrho GTP-Binding ProteinsSignal TransductionTransforming Growth Factor beta1extra domain A fibronectin, humanFibronectinsIntegrinsrho GTP-Binding ProteinsTransforming Growth Factor beta1EDA-FNExtracellular matrixMyofibroblastPositive feedback loopTGF-β1

Identifiers

PMID30184544
PMCPMC6611700
OpenAlexW2889965700

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.