Evidence map›Paper›PMID 36053751›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2022

Mechanical response of cardiac microtissues to acute localized injury.

Shoshana L Das, Bryan P Sutherland, Emma Lejeune, Jeroen Eyckmans, Christopher S Chen

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Suspended Tissue Open Microfluidic Patterning (STOMP).Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  5. Article
  6. Article
  7. Suspended Tissue Open Microfluidic Patterning (STOMP).bioRxiv : the preprint server for biology · 2025
    Article
  8. Dressed in Collagen: 2D and 3D Cardiac Fibrosis Models.International journal of molecular sciences · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. Dynamic control of contractile resistance to iPSC-derived micro-heart muscle arrays.Journal of biomedical materials research. Part A · 2024
    Article
  13. Article
  14. Article
  15. Engineered Heart Tissues for Standard 96-Well Tissue Culture Plates.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  16. Article
  17. Review
  18. High throughput screening system for engineered cardiac tissues.Frontiers in bioengineering and biotechnology · 2023
    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

5 authors at 1 institution in 1 country.

Shoshana L DasHarvard-MIT Program in Health Sciences and Technology, Institute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, Massachusetts.ORCID 0000-0003-1328-3137
Bryan P SutherlandDepartment of Biomedical Engineering, Boston University, Boston, Massachusetts.
Emma LejeuneDepartment of Mechanical Engineering, Boston University, Boston, Massachusetts.ORCID 0000-0001-8099-3468
Jeroen EyckmansDepartment of Biomedical Engineering, Boston University, Boston, Massachusetts.
Christopher S ChenDepartment of Biomedical Engineering, Boston University, Boston, Massachusetts.ORCID 0000-0003-2445-8449
Boston University · US

Funding

Development of a wound-on-chip model to study stromal-epithelial interactions during tissue repairR21EB028491 · NIBIB · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI EYCKMANS, JEROEN · 2020 to 2022
$660k
6 · The paper itself

Abstract

After a myocardial infarction (MI), the heart undergoes changes including local remodeling that can lead to regional abnormalities in mechanical and electrical properties, ultimately increasing the risk of arrhythmias and heart failure. Although these responses have been successfully recapitulated in animal models of MI, local changes in tissue and cell-level mechanics caused by MI remain difficult to study in vivo. Here, we developed an in vitro cardiac microtissue (CMT) injury system that through acute focal injury recapitulates aspects of the regional responses seen following an MI. With a pulsed laser, cell death was induced in the center of the microtissue causing a loss of calcium signaling and a complete loss of contractile function in the injured region and resulting in a 39% reduction in the CMT's overall force production. After 7 days, the injured area remained void of cardiomyocytes (CMs) and showed increased expression of vimentin and fibronectin, two markers for fibrotic remodeling. Interestingly, although the injured region showed minimal recovery, calcium amplitudes in uninjured regions returned to levels comparable with control. Furthermore, overall force production returned to preinjury levels despite the lack of contractile function in the injured region. Instead, uninjured regions exhibited elevated contractile function, compensating for the loss of function in the injured region, drawing parallels to changes in tissue-level mechanics seen in vivo. Overall, this work presents a new in vitro model to study cardiac tissue remodeling and electromechanical changes after injury.

Indexed as

FibronectinsMyocardial InfarctionAnimalsCalciumDisease Models, AnimalHumansMyocytes, CardiacVentricular RemodelingVimentinCalciumFibronectinsVimentincardiac fibrosiscardiac mechanicscardiac tissue engineeringiPSC-derived cardiomyocytesorgan-on-chip

Identifiers

PMID36053751
PMCPMC9662801
OpenAlexW4294300881

What Socratic 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 Socratic graph.