Evidence map›Paper›PMID 28993153›Full record

ArticleJournal of molecular and cellular cardiology2017

TFEB activation protects against cardiac proteotoxicity via increasing autophagic flux.

Bo Pan, Hanming Zhang, Taixing Cui, Xuejun Wang

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing 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

60 citing papers in PubMed, 93 citations in OpenAlex.

  1. Article
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  4. The R120G knock-in mutation in αB-crystallin is insufficient to induce cardiomyopathy in mice.American journal of physiology. Heart and circulatory physiology · 2026
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  18. Regulation of autophagy of the heart in ischemia and reperfusion.Apoptosis : an international journal on programmed cell death · 2023
    Review
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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

4 authors at 2 institutions in 1 country.

Bo PanDivision of Basic Biomedical sciences, University of South Dakota Sanford School of Medicine, Vermillion, SD 57069, USA.
Hanming ZhangDivision of Basic Biomedical sciences, University of South Dakota Sanford School of Medicine, Vermillion, SD 57069, USA.
Taixing CuiDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC 29209, USA.
Xuejun WangDivision of Basic Biomedical sciences, University of South Dakota Sanford School of Medicine, Vermillion, SD 57069, USA. Electronic address: xuejun.wang@usd.edu.
University of South Dakota · USUniversity of South Carolina · US

Funding

Use of Resveratrol to treat experimental multiple sclerosisP01AT003961 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI NAGARKATTI, PRAKASH S · 2007 to 2018
$14.2M
Ubiquitin receptors and cardiac proteotoxicityR01HL072166 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI WANG, XUEJUN · 2003 to 2023
$6.9M
The COP9 SIgnalosome in the HeartR01HL085629 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI WANG, XUEJUN · 2006 to 2019
$4.7M
The NRF2-p62 Axis in the Cross-Talk between Proteasomal and Lysosomal DegradationR01HL131667 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI CUI, TAIXING, WANG, XUEJUN · 2017 to 2020
$1.4M
NCCIH NIH HHS P01 AT003961NHLBI NIH HHS R01 HL072166NHLBI NIH HHS R01 HL085629NHLBI NIH HHS R01 HL131667
6 · The paper itself

Abstract

Insufficient lysosomal removal of autophagic cargoes in cardiomyocytes has been suggested as a main cause for the impairment of the autophagic-lysosomal pathway (ALP) in many forms of heart disease including cardiac proteinopathy and may play an important pathogenic role; however, the molecular basis and the correcting strategy for the cardiac ALP insufficiency require further investigation. The present study was sought to determine whether myocardial expression and activity of TFEB, the recently identified ALP master regulator, are impaired in a cardiac proteinopathy mouse model and to determine the effect of genetic manipulation of TFEB expression on autophagy and proteotoxicity in a cardiomyocyte model of proteinopathy. We found that increased myocardial TFEB mRNA levels and a TFEB protein isoform switch were associated with marked decreases in the mRNA levels of representative TFEB target genes and increased mTORC1 activation, in mice with cardiac transgenic expression of a missense (R120G) mutant αB-crystallin (CryAB

Indexed as

alpha-Crystallin B ChainAnimalsAutophagyBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCell SurvivalFemaleHeart DiseasesHeart VentriclesLysosomesMaleMechanistic Target of Rapamycin Complex 1MiceMice, TransgenicMyocytes, CardiacRatsRats, Sprague-Dawleyalpha-Crystallin B ChainBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsMechanistic Target of Rapamycin Complex 1RNA, MessengerCardiomyocytesMisfolded proteinsmTORProteotoxicityTFEBThe autophagic-lysosomal pathway

Identifiers

PMID28993153
PMCPMC5656243
OpenAlexW2763986177

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.