Evidence map›Paper›PMID 32085622›Full record

ArticleInternational journal of molecular sciences2020

The ER Unfolded Protein Response Effector, ATF6, Reduces Cardiac Fibrosis and Decreases Activation of Cardiac Fibroblasts.

Winston T Stauffer, Erik A Blackwood, Khalid Azizi, Randal J Kaufman, Christopher C Glembotski

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 28 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

5 authors at 2 institutions in 1 country.

Winston T StaufferDepartment of Biology, San Diego State University Heart Institute, San Diego State University, San Diego, CA 92182, USA.
Erik A BlackwoodDepartment of Biology, San Diego State University Heart Institute, San Diego State University, San Diego, CA 92182, USA.
Khalid AziziDepartment of Biology, San Diego State University Heart Institute, San Diego State University, San Diego, CA 92182, USA.
Randal J KaufmanDegenerative Diseases Program, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA.
Christopher C GlembotskiDepartment of Biology, San Diego State University Heart Institute, San Diego State University, San Diego, CA 92182, USA.
San Diego State University · USDiscovery Institute · US

Funding

"A Novel Role for the UPR Component, ATF6 in AD-associated Neuroprotective Pathways"R01AG062190 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI HUANG, TIMOTHY YIKAI, KAUFMAN, RANDAL J. · 2019 to 2023
$4.8M
ER stress and UPR in non-alcoholic steatohepatitis and hepatocellular carcinomaR01CA198103 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI KAUFMAN, RANDAL J. · 2016 to 2020
$3.4M
Mechanism of ER Protein Misfolding-Induced Mitochondrial DysfunctionR01DK113171 · NIDDK · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI KAUFMAN, RANDAL J. · 2017 to 2020
$2.5M
The ER Stress-Induced Selenoprotein, SelenoS, Regulates Proteostasis and Cardiac HypertrophyR01HL149931 · NHLBI · UNIVERSITY OF ARIZONA · PI GLEMBOTSKI, CHRIS · 2020 to 2023
$1.7M
Harnessing the Adaptive ER Stress Response in Myocardial IschemiaR01HL135893 · NHLBI · UNIVERSITY OF ARIZONA · PI GLEMBOTSKI, CHRIS · 2017 to 2020
$1.5M
ATF6 is Required for ANP Secretion from the HeartR01HL141463 · NHLBI · UNIVERSITY OF ARIZONA · PI GLEMBOTSKI, CHRIS · 2019 to 2022
$1.5M
The Adaptive Cardiac Sensor, ATF6, Regulates ANP Secretion and Decreases Hypertensive StressF31HL140850 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI BLACKWOOD, ERIK · 2018 to 2020
$69k
National Heart and Lung Institute 1F31HL140850, R01HL135893, R01 HL75573, and R01 HL104535NCI NIH HHS R01 CA198103NHLBI NIH HHS R01 HL135893NHLBI NIH HHS R01 HL141463NHLBI NIH HHS R01 HL149931NIA NIH HHS R01 AG062190NIDDK NIH HHS R01 DK113171
6 · The paper itself

Abstract

Activating transcription factor-6 α (ATF6) is one of the three main sensors and effectors of the endoplasmic reticulum (ER) stress response and, as such, it is critical for protecting the heart and other tissues from a variety of environmental insults and disease states. In the heart, ATF6 has been shown to protect cardiac myocytes. However, its roles in other cell types in the heart are unknown. Here we show that ATF6 decreases the activation of cardiac fibroblasts in response to the cytokine, transforming growth factor β (TGFβ), which can induce fibroblast trans-differentiation into a myofibroblast phenotype through signaling via the TGFβ-Smad pathway. ATF6 activation suppressed fibroblast contraction and the induction of α smooth muscle actin (αSMA). Conversely, fibroblasts were hyperactivated when ATF6 was silenced or deleted. ATF6 thus represents a novel inhibitor of the TGFβ-Smad axis of cardiac fibroblast activation.

Indexed as

Unfolded Protein ResponseActivating Transcription Factor 6AnimalsBiomarkersEndoplasmic ReticulumFibroblastsFibrosisGene Expression RegulationHeart VentriclesMaleMice, Inbred C57BLMice, KnockoutModels, BiologicalMyocardiumPhosphorylationSignal TransductionActivating Transcription Factor 6Atf6 protein, mouseBiomarkersSmad2 ProteinTransforming Growth Factor betaATF6cardiac fibroblastcardiac fibrosisendoplasmic reticulumER stressSmadTGFβUPR

Identifiers

PMID32085622
PMCPMC7073073
OpenAlexW3008264268

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.