Evidence map›Paper›PMID 31406913›Full record

ArticleAdvanced biosystems2018

Mechanoregulation of Myofibroblast Fate and Cardiac Fibrosis.

Peter Kim, Nick Chu, Jennifer Davis, Deok-Ho Kim

Abstract read
In one paragraph

Article in Advanced biosystems, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Cytotoxic CD4Signal transduction and targeted therapy · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Atrial Fibrillation: Pathogenesis, Predisposing Factors, and Genetics.International journal of molecular sciences · 2021
    Review
  10. Review
  11. Review
  12. Review
  13. Review
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 2 countries.

Peter KimDepartment of Bioengineering, University of Washington, Seattle, WA 98109, USA.
Nick ChuDepartment of Bioengineering, University of Washington, Seattle, WA 98109, USA.
Jennifer DavisDepartment of Bioengineering, University of Washington, Seattle, WA 98109, USA.
Deok-Ho KimDepartment of Bioengineering, University of Washington, Seattle, WA 98109, USA.
University of Washington · USCalifornia Institute for Regenerative Medicine · US

Funding

A NANOPATTERNED MEA-BASED FUNCTIONAL PHENOTYPING ASSAY FOR DRUG-INDUCED CARDIOTOXICITY SCREENINGR01HL135143 · NHLBI · UNIVERSITY OF WASHINGTON · PI KIM, DEOK-HO · 2017 to 2021
$1.9M
MBNL1's function in myofibroblast transformation and fibrosisR00HL119353 · NHLBI · UNIVERSITY OF WASHINGTON · PI DAVIS, JENNIFER MICHELLE · 2015 to 2017
$747k
Injectable myocardial matrix-grapheme composite hydrogels for functional cardiac tissue engineeringR21EB020132 · NIBIB · UNIVERSITY OF WASHINGTON · PI KIM, DEOK-HO · 2016 to 2017
$435k
NHLBI NIH HHS R00 HL119353NHLBI NIH HHS R01 HL135143NIBIB NIH HHS R21 EB020132
6 · The paper itself

Abstract

During myocardial infarction, myocytes die and are replaced by a specialized fibrotic extracellular matrix, otherwise known as scarring. Fibrotic scarring presents a tremendous hemodynamic burden on the heart, as it creates a stiff substrate, which resists diastolic filling. Fibrotic mechanisms result in permanent scarring which often leads to hypertrophy, arrhythmias, and a rapid progression to failure. Despite the deep understanding of fibrosis in other tissues, acquired through previous investigations, the mechanisms of cardiac fibrosis remain unclear. Recent studies suggest that biochemical cues as well as mechanical cues regulate cells in myocardium. However, the steps in myofibroblast transdifferentiation, as well as the molecular mechanisms of such transdifferentiation in vivo, are poorly understood. This review is focused on defining myofibroblast physiology, scar mechanics, and examining current findings of myofibroblast regulation by mechanical stress, stiffness, and topography for understanding fibrotic disease dynamics.

Indexed as

biomechanicscardiac engineeringfibrosismechanoregulationmyofibroblasts

Identifiers

PMID31406913
PMCPMC6690497
OpenAlexW2773474962

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.