Evidence map›Paper›PMID 34041746›Full record

ArticleJournal of cellular physiology2021

Effects of emodin, a plant-derived anthraquinone, on TGF-β1-induced cardiac fibroblast activation and function.

Wayne Carver, Ethan Fix, Charity Fix, Daping Fan, Mrinmay Chakrabarti, Mohamad Azhar

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Wayne CarverDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina, USA.ORCID 0000-0002-7699-6241
Ethan FixDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina, USA.
Charity FixDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina, USA.
Daping FanDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina, USA.
Mrinmay ChakrabartiDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina, USA.
Mohamad AzharDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina, USA.
University of South Carolina · US

Funding

Medial Arterial Calcification: Mechanisms and TherapyR01HL145064 · NHLBI · CLEMSON UNIVERSITY · PI VYAVAHARE, NAREN R · 2019 to 2022
$2.3M
Emodin as a chemopreventive agent for breast cancer - admin suppR01CA218578 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI FAN, DAPING, MURPHY, ELIZABETH ANGELA · 2018 to 2022
$1.9M
Analysis of TGFbeta ligands function in heart development and diseaseR01HL126705 · NHLBI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI AZHAR, MOHAMAD · 2015 to 2018
$1.4M
American Heart Association-American Stroke Association 17GRNT33650018NCI NIH HHS R01 CA218578NCI NIH HHS R01CA218578NHLBI NIH HHS R01 HL126705NHLBI NIH HHS R01HL126705NHLBI NIH HHS R01 HL145064NHLBI NIH HHS R01HL145064
6 · The paper itself

Abstract

Cardiac fibrosis accompanies a number of pathological conditions and results in altered myocardial structure, biomechanical properties and function. The signaling networks leading to fibrosis are complex, contributing to the general lack of progress in identifying effective therapeutic approaches to prevent or reverse this condition. Several studies have shown protective effects of emodin, a plant-derived anthraquinone, in animal models of fibrosis. A number of questions remain regarding the mechanisms whereby emodin impacts fibrosis. Transforming growth factor beta 1 (TGF-β1) is a potent stimulus of fibrosis and fibroblast activation. In the present study, experiments were performed to evaluate the effects of emodin on activation and function of cardiac fibroblasts following treatment with TGF-β1. We demonstrate that emodin attenuates TGF-β1-induced fibroblast activation and collagen accumulation in vitro. Emodin also inhibits activation of several canonical (SMAD2/3) and noncanonical (Erk1/2) TGF-β signaling pathways, while activating the p38 pathway. These results suggest that emodin may provide an effective therapeutic agent for fibrosis that functions via specific TGF-β signaling pathways.

Indexed as

AnimalsCell MovementCell ProliferationCells, CulturedCollagenEmodinFibroblastsFibrosisMaleMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Myocardiump38 Mitogen-Activated Protein KinasesRatsRats, Sprague-DawleySignal TransductionCollagenEmodinMapk1 protein, ratMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3p38 Mitogen-Activated Protein KinasesSmad2 ProteinSmad2 protein, ratSmad3 ProteinSmad3 protein, ratTransforming Growth Factor beta1emodinfibroblastfibrosisTGF-β

Identifiers

PMID34041746
PMCPMC8530838
OpenAlexW3165117636

What OpenQuestion holds

Textmetadata
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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.