Evidence map›Paper›PMID 27714411›Full record

ReviewCellular and molecular life sciences : CMLS2017

How cardiomyocytes sense pathophysiological stresses for cardiac remodeling.

Zaffar K Haque, Da-Zhi Wang

Abstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
–field-weighted citation impact
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

39 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. The βCirculation research · 2025
    Article
  5. Article
  6. Article
  7. YTHDF1 is pivotal for maintenance of cardiac homeostasis.Journal of molecular and cellular cardiology · 2024
    Article
  8. Article
  9. Article
  10. Mast Cells in Cardiac Remodeling: Focus on the Right Ventricle.Journal of cardiovascular development and disease · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Loss of YTHDF2 Alters the Expression of mJACC. Basic to translational science · 2023
    Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  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

2 authors.

Zaffar K HaqueDepartment of Cardiology, Boston Children's Hospital, Harvard Medical School, 1260 John F. Enders Research Bldg, 320 Longwood Ave, Boston, MA, 02115, USA. zhaque01@yahoo.com.
Da-Zhi WangDepartment of Cardiology, Boston Children's Hospital, Harvard Medical School, 1260 John F. Enders Research Bldg, 320 Longwood Ave, Boston, MA, 02115, USA.

Funding

RESEARCH METHODS IN PEDIATRICS HEART DISEASET32HL007572 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI Sarah D DE FERRANTI, Jane W. Newburger · 1985 to 2026
$13.0M
MicroRNAs, cardiac development and functionR01HL085635 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WANG, DA-ZHI · 2007 to 2015
$3.2M
Therapeutic applications of miRNAs in myocardial and cardiac regenerationR01HL125925 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI WANG, DA-ZHI · 2016 to 2019
$1.8M
Molecular Mechanisms of Dilated CardiomyopathyR01HL116919 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI WANG, DA-ZHI · 2013 to 2016
$1.7M
NHLBI NIH HHS R01 HL085635NHLBI NIH HHS R01 HL116919NHLBI NIH HHS R01 HL125925NHLBI NIH HHS T32 HL007572
6 · The paper itself

Abstract

In the past decades, the cardiovascular community has laid out the fundamental signaling cascades that become awry in the cardiomyocyte during the process of pathologic cardiac remodeling. These pathways are initiated at the cell membrane and work their way to the nucleus to mediate gene expression. Complexity is multiplied as the cardiomyocyte is subjected to cross talk with other cells as well as a barrage of extracellular stimuli and mechanical stresses. In this review, we summarize the signaling cascades that play key roles in cardiac function and then we proceed to describe emerging concepts of how the cardiomyocyte senses the mechanical and environmental stimuli to transition to the deleterious genetic program that defines pathologic cardiac remodeling. As a highlighting example of these processes, we illustrate the transition from a compensated hypertrophied myocardium to a decompensated failing myocardium, which is clinically manifested as decompensated heart failure.

Indexed as

Stress, PhysiologicalVentricular RemodelingAnimalsCardiomegalyHeart FailureHumansMyocytes, CardiacSignal TransductionCardiomyopathyGene expressionHeart failureMicroRNAsSignaling pathwayTranscription

Identifiers

PMID27714411
PMCPMC6990138

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Registered trials

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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.