Evidence map›Paper›PMID 34674743›Full record

ArticleJournal of biological engineering2021

AZD2014, a dual mTOR inhibitor, attenuates cardiac hypertrophy in vitro and in vivo.

Byung-Hyun Cha, Minjin Jung, Angela S Kim, Victoria C Lepak, Brett A Colson, David A Bull, Youngwook Won

Open access · goldAbstract read
In one paragraph

Article in Journal of biological engineering, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 41% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
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

7 authors at 1 institution in 1 country.

Byung-Hyun ChaDivision of Cardio-Thoracic Surgery, Department of Surgery, University of Arizona College of Medicine, Tucson, AZ, 85724, USA.
Minjin JungDivision of Cardio-Thoracic Surgery, Department of Surgery, University of Arizona College of Medicine, Tucson, AZ, 85724, USA.
Angela S KimDivision of Cardio-Thoracic Surgery, Department of Surgery, University of Arizona College of Medicine, Tucson, AZ, 85724, USA.
Victoria C LepakDepartment of Cellular & Molecular Medicine, University of Arizona College of Medicine, Tucson, AZ, 85724, USA.
Brett A ColsonDepartment of Cellular & Molecular Medicine, University of Arizona College of Medicine, Tucson, AZ, 85724, USA.
David A BullDivision of Cardio-Thoracic Surgery, Department of Surgery, University of Arizona College of Medicine, Tucson, AZ, 85724, USA.
Youngwook WonDivision of Cardio-Thoracic Surgery, Department of Surgery, University of Arizona College of Medicine, Tucson, AZ, 85724, USA. youngwookwon@email.arizona.edu.
University of Arizona · US

Funding

PHYSIOLOGYT32HL007249 · NHLBI · UNIVERSITY OF ARIZONA · PI Brett A Colson, JOHN P KONHILAS · 1985 to 2026
$12.5M
Structural Dynamics of Cardiac Myosin-Binding Protein C RegulationR01HL141564 · NHLBI · UNIVERSITY OF ARIZONA · PI Brett A Colson · 2019 to 2026
$3.8M
Targeted Systemic Delivery of SDF-1 DNA for the Treatment of Chronic Heart DiseaseR01HL138242 · NHLBI · UNIVERSITY OF NORTH TEXAS · PI WON, YOUNG-WOOK · 2017 to 2021
$2.3M
Foundation for the National Institutes of Health R01HL138242Foundation for the National Institutes of Health R01HL141564NHLBI NIH HHS R01 HL138242NHLBI NIH HHS R01 HL141564NHLBI NIH HHS T32 HL007249
6 · The paper itself

Abstract

Cardiac hypertrophy is one of the most common genetic heart disorders and considered a risk factor for cardiac morbidity and mortality. The mammalian target of rapamycin (mTOR) pathway plays a key regulatory function in cardiovascular physiology and pathology in hypertrophy. AZD2014 is a small-molecule ATP competitive mTOR inhibitor working on both mTORC1 and mTORC2 complexes. Little is known about the therapeutic effects of AZD2014 in cardiac hypertrophy and its underlying mechanism. Here, AZD2014 is examined in in vitro model of phenylephrine (PE)-induced human cardiomyocyte hypertrophy and a myosin-binding protein-C (Mybpc3)-targeted knockout (KO) mouse model of cardiac hypertrophy. Our results demonstrate that cardiomyocytes treated with AZD2014 retain the normal phenotype and AZD2014 attenuates cardiac hypertrophy in the Mybpc3-KO mouse model through inhibition of dual mTORC1 and mTORC2, which in turn results in the down-regulation of the Akt/mTOR signaling pathway.

Indexed as

AZD2014Cardiac hypertrophyCardiomyocytemTOR inhibitor

Identifiers

PMID34674743
PMCPMC8529824
OpenAlexW3149181357

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.