Evidence map›Paper›PMID 35026670›Full record

ArticleBiomaterials2022

Cardiac ischemia on-a-chip to investigate cellular and molecular response of myocardial tissue under hypoxia.

Jaimeson Veldhuizen, Ramani Chavan, Babak Moghadas, Jin G Park, Vikram D Kodibagkar, Raymond Q Migrino, Mehdi Nikkhah

Open access · greenAbstract read
In one paragraph

Article in Biomaterials, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 74 citations in OpenAlex.

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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 2 institutions in 1 country.

Jaimeson VeldhuizenSchool of Biological and Health Systems Engineering (SBHSE), Arizona State University, Tempe, AZ, 85287, USA.
Ramani ChavanCenter for Personalized Diagnostics (CPD), Biodesign Institute, Arizona State University, Tempe, AZ, 85287, USA.
Babak MoghadasSchool of Biological and Health Systems Engineering (SBHSE), Arizona State University, Tempe, AZ, 85287, USA.
Jin G ParkCenter for Personalized Diagnostics (CPD), Biodesign Institute, Arizona State University, Tempe, AZ, 85287, USA.
Vikram D KodibagkarSchool of Biological and Health Systems Engineering (SBHSE), Arizona State University, Tempe, AZ, 85287, USA.
Raymond Q MigrinoPhoenix Veterans Affairs Health Care System, Phoenix, AZ, 85012, USA; University of Arizona College of Medicine, Phoenix, AZ, 85004, USA.
Mehdi NikkhahSchool of Biological and Health Systems Engineering (SBHSE), Arizona State University, Tempe, AZ, 85287, USA; Center for Personalized Diagnostics (CPD), Biodesign Institute, Arizona State University, Tempe, AZ, 85287, USA. Electronic address: mnikkhah@asu.edu.
Arizona State University · USPhoenix VA Health Care System · US

Funding

Leica TCS SP8 Laser Scanning Confocal MicroscopeS10OD023691 · OD · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · PI BALUCH, DEBRA PAGE · 2017 to 2017
$600k
NIH HHS S10 OD023691
6 · The paper itself

Abstract

Tissue engineering has enabled the development of advanced and physiologically relevant models of cardiovascular diseases, with advantages over conventional 2D in vitro assays. We have previously demonstrated development of a heart on-a-chip microfluidic model with mature 3D anisotropic tissue formation that incorporates both stem cell-derived cardiomyocytes and cardiac fibroblasts within a collagen-based hydrogel. Using this platform, we herein present a model of myocardial ischemia on-a-chip, that recapitulates ischemic insult through exposure of mature 3D cardiac tissues to hypoxic environments. We report extensive validation and molecular-level analyses of the model in its ability to recapitulate myocardial ischemia in response to hypoxia, demonstrating the 1) induction of tissue fibrosis through upregulation of contractile fibers, 2) dysregulation in tissue contraction through functional assessment, 3) upregulation of hypoxia-response genes and downregulation of contractile-specific genes through targeted qPCR, and 4) transcriptomic pathway regulation of hypoxic tissues. Further, we investigated the complex response of ischemic myocardial tissues to reperfusion, identifying 5) cell toxicity, 6) sustained contractile irregularities, as well as 7) re-establishment of lactate levels and 8) gene expression, in hypoxic tissues in response to ischemia reperfusion injury.

Indexed as

Lab-On-A-Chip DevicesMyocardial IschemiaHumansHypoxiaMyocardiumMyocytes, CardiacCardiacEngineeredHeart-on-a-chipIschemiaMicrofluidicStem cell

Identifiers

PMID35026670
PMCPMC10440189
OpenAlexW4200533588

What OpenQuestion holds

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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.