Evidence map›Paper›PMID 32517807›Full record

ReviewCell communication and signaling : CCS2020

TGF-β and WNT signaling pathways in cardiac fibrosis: non-coding RNAs come into focus.

Fatemeh Yousefi, Zahra Shabaninejad, Sina Vakili, Maryam Derakhshan, Ahmad Movahedpour, Hamed Dabiri, Younes Ghasemi, Maryam Mahjoubin-Tehran, Azin Nikoozadeh, Amir Savardashtaki and 2 more

Open access · goldAbstract readReviewVideo-Audio Media
In one paragraph

Review in Cell communication and signaling : CCS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
17.5field-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

110 citing papers in PubMed, 184 citations in OpenAlex.

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50 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

12 authors at 6 institutions in 2 countries.

Fatemeh YousefiDepartment of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran.
Zahra ShabaninejadDepartment of Nanotechnology, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran.
Sina VakiliBiochemistry Department, Medical School, Shiraz University of Medical Sciences, Shiraz, Iran.
Maryam DerakhshanDepartment of Pathology, Isfahan University of Medical Sciences, Isfahan, Iran.
Ahmad MovahedpourDepartment of Medical Biotechnology, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran.
Hamed DabiriDepartment of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran.
Younes GhasemiPharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Maryam Mahjoubin-TehranStudent Research Committee, Mashhad University of Medical Sciences, Mashhad, Iran.
Azin NikoozadehPathology Department, School of Medicine,Mashhad Univesity of Medical Sciences, Mashhad, Iran.
Amir SavardashtakiPharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Dashtaki63@gmail.com.
Hamed MirzaeiResearch Center for Biochemistry and Nutrition in Metabolic Diseases, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, IR, Iran. HAMBLIN@helix.mgh.harvard.edu.
Michael R HamblinWellman Center for Photomedicine, Massachusetts General Hospital, Harvard Medical School, 40 Blossom Street, Boston, MA, 02114, USA. mirzaei-h@kaums.ac.ir.
Shiraz University of Medical Sciences · IRTarbiat Modares University · IRMashhad University of Medical Sciences · IRIsfahan University of Medical Sciences · IRKashan University of Medical Sciences · IRMassachusetts General Hospital · US

Funding

Photodynamic Therapy of Localized InfectionsR01AI050875 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI HAMBLIN, MICHAEL R · 2003 to 2017
$4.8M
Synergistic Photodynamic Therapy for Catherer-Associated Urinary Tract InfectionsR21AI121700 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI HAMBLIN, MICHAEL R · 2016 to 2017
$462k
NIAID NIH HHS R01 AI050875NIAID NIH HHS R21 AI121700
6 · The paper itself

Abstract

Cardiac fibrosis describes the inappropriate proliferation of cardiac fibroblasts (CFs), leading to accumulation of extracellular matrix (ECM) proteins in the cardiac muscle, which is found in many pathophysiological heart conditions. A range of molecular components and cellular pathways, have been implicated in its pathogenesis. In this review, we focus on the TGF-β and WNT signaling pathways, and their mutual interaction, which have emerged as important factors involved in cardiac pathophysiology. The molecular and cellular processes involved in the initiation and progression of cardiac fibrosis are summarized. We focus on TGF-β and WNT signaling in cardiac fibrosis, ECM production, and myofibroblast transformation. Non-coding RNAs (ncRNAs) are one of the main players in the regulation of multiple pathways and cellular processes. MicroRNAs, long non-coding RNAs, and circular long non-coding RNAs can all interact with the TGF-β/WNT signaling axis to affect cardiac fibrosis. A better understanding of these processes may lead to new approaches for diagnosis and treatment of many cardiac conditions. Video Abstract.

Indexed as

Wnt Signaling PathwayAnimalsFibrosisHumansMyocardiumMyofibroblastsRNA, UntranslatedTransforming Growth Factor betaRNA, UntranslatedTransforming Growth Factor betaCardiac fibrosisNon-coding RNAsTGF-β/WNT signaling

Identifiers

PMID32517807
PMCPMC7281690
OpenAlexW3033500181

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.