Evidence map›Paper›PMID 28246202›Full record

ArticleScience signaling2017

DDiT4L promotes autophagy and inhibits pathological cardiac hypertrophy in response to stress.

Bridget Simonson, Vinita Subramanya, Mun Chun Chan, Aifeng Zhang, Hannabeth Franchino, Filomena Ottaviano, Manoj K Mishra, Ashley C Knight, Danielle Hunt, Ionita Ghiran and 4 more

Open access · greenAbstract read
In one paragraph

Article in Science signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

14 authors at 3 institutions in 1 country.

Bridget SimonsonCardiovascular Research Center, Massachusetts General Hospital, Boston, MA 02114, USA.ORCID 0000-0002-3190-4796
Vinita SubramanyaCardiovascular Research Institute, Beth Israel Deaconess Medical Center, Boston, MA 02115, USA.
Mun Chun ChanCardiovascular Research Center, Massachusetts General Hospital, Boston, MA 02114, USA.
Aifeng ZhangCardiovascular Research Center, Massachusetts General Hospital, Boston, MA 02114, USA.
Hannabeth FranchinoCardiovascular Research Institute, Beth Israel Deaconess Medical Center, Boston, MA 02115, USA.
Filomena OttavianoCardiovascular Research Institute, Beth Israel Deaconess Medical Center, Boston, MA 02115, USA.ORCID 0000-0003-1540-7447
Manoj K MishraDepartment of Physiology, Pennsylvania Muscle Institute, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Ashley C KnightCardiovascular Research Institute, Beth Israel Deaconess Medical Center, Boston, MA 02115, USA.
Danielle HuntCardiovascular Research Institute, Beth Israel Deaconess Medical Center, Boston, MA 02115, USA.ORCID 0000-0002-3557-4915
Ionita GhiranCardiovascular Research Institute, Beth Israel Deaconess Medical Center, Boston, MA 02115, USA.ORCID 0000-0001-6655-3298
Tejvir S KhuranaDepartment of Physiology, Pennsylvania Muscle Institute, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Maria I KontaridisCardiovascular Research Institute, Beth Israel Deaconess Medical Center, Boston, MA 02115, USA.
Anthony RosenzweigCardiovascular Research Center, Massachusetts General Hospital, Boston, MA 02114, USA.
Saumya DasCardiovascular Research Center, Massachusetts General Hospital, Boston, MA 02114, USA. sdas@partners.org.ORCID 0000-0002-4521-4606
Beth Israel Deaconess Medical Center · USMassachusetts General Hospital · USUniversity of Pennsylvania · US

Funding

STRUCTURE-FUNCTION RELATIONSHIPS IN THE ALIMENTARY TRACTP30DK034854 · NIDDK · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WAYNE I LENCER · 1986 to 2026
$32.4M
The Role of RhoA in the Molecular Pathogenesis of Heart DiseaseR01HL102368 · NHLBI · MASONIC MEDICAL RESEARCH LABORATORY, INC · PI KONTARIDIS, MARIA I · 2010 to 2021
$5.1M
Targeted inhibition of fibrosis for the prevention of heart failureR01HL122238 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI MCCARTHY, JASON R. · 2015 to 2019
$4.0M
Novel Role for Circulating extracellular RNAs in Human Heart FailureR01HL122547 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI DAS, SAUMYA · 2015 to 2019
$2.1M
Role of serum- and glucocorticoid-regulated kinase-1 in electrical remodelingR01HL094677 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROSENZWEIG, ANTHONY · 2010 to 2013
$1.7M
Elucidating the Phosphatase-Independent Roles of PTPN11 in the HeartR01HL114775 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KONTARIDIS, MARIA I · 2013 to 2016
$1.7M
Role of miR-222 in pathological hypertrophy and heart failureR01HL135886 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI ROSENZWEIG, ANTHONY · 2017 to 2020
$1.7M
NHLBI NIH HHS R01 HL094677NHLBI NIH HHS R01 HL102368NHLBI NIH HHS R01 HL114775NHLBI NIH HHS R01 HL122238NHLBI NIH HHS R01 HL122547NHLBI NIH HHS R01 HL135886NIDDK NIH HHS P30 DK034854
6 · The paper itself

Abstract

Physiological cardiac hypertrophy, in response to stimuli such as exercise, is considered adaptive and beneficial. In contrast, pathological cardiac hypertrophy that arises in response to pathological stimuli such as unrestrained high blood pressure and oxidative or metabolic stress is maladaptive and may precede heart failure. We found that the transcript encoding DNA damage-inducible transcript 4-like (DDiT4L) was expressed in murine models of pathological cardiac hypertrophy but not in those of physiological cardiac hypertrophy. In cardiomyocytes, DDiT4L localized to early endosomes and promoted stress-induced autophagy through a process involving mechanistic target of rapamycin complex 1 (mTORC1). Exposing cardiomyocytes to various types of pathological stress increased the abundance of

Indexed as

Gene Expression RegulationAdaptor Proteins, Signal TransducingAnimalsAnimals, NewbornAutophagyBlotting, WesternCardiomegalyCells, CulturedDNA-Binding ProteinsEndosomesHEK293 CellsHumansMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2Mice, KnockoutMice, TransgenicAdaptor Proteins, Signal TransducingDdit4l protein, mouseDNA-Binding ProteinsMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2Transcription Factors

Identifiers

PMID28246202
PMCPMC5509050
OpenAlexW2594551384

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.