Evidence map›Paper›PMID 37032398›Full record

ArticleAnnals of biomedical engineering2023

Myocardial Biomechanics and the Consequent Differentially Expressed Genes of the Left Atrial Ligation Chick Embryonic Model of Hypoplastic Left Heart Syndrome.

S Samaneh Lashkarinia, Wei Xuan Chan, Efthymios Motakis, Sheldon Ho, Hummaira Banu Siddiqui, Mervenur Coban, Bortecine Sevgin, Kerem Pekkan, Choon Hwai Yap

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Article in Annals of biomedical engineering, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

5 citing papers in PubMed, 8 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

9 authors at 4 institutions in 4 countries.

S Samaneh LashkariniaDepartment of Bioengineering, Imperial College London, South Kensington Campus, London, UK.
Wei Xuan ChanDepartment of Bioengineering, Imperial College London, South Kensington Campus, London, UK.
Efthymios MotakisThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA.
Sheldon HoDepartment of Biomedical Engineering, National University of Singapore, Singapore, Singapore.
Hummaira Banu SiddiquiDepartment of Mechanical Engineering, Koc University, Istanbul, Turkey.
Mervenur CobanDepartment of Mechanical Engineering, Koc University, Istanbul, Turkey.
Bortecine SevginDepartment of Mechanical Engineering, Koc University, Istanbul, Turkey.
Kerem PekkanDepartment of Mechanical Engineering, Koc University, Istanbul, Turkey.
Choon Hwai YapDepartment of Bioengineering, Imperial College London, South Kensington Campus, London, UK. c.yap@imperial.ac.uk.ORCID http://orcid.org/0000-0003-2918-3077
Koç University · TRImperial College London · GBJackson Laboratory · USNational University of Singapore · SG

Funding

Imperial College London Startup FundingRoyal Society NIF\R1\202197
6 · The paper itself

Abstract

Left atrial ligation (LAL) of the chick embryonic heart is a model of the hypoplastic left heart syndrome (HLHS) where a purely mechanical intervention without genetic or pharmacological manipulation is employed to initiate cardiac malformation. It is thus a key model for understanding the biomechanical origins of HLHS. However, its myocardial mechanics and subsequent gene expressions are not well-understood. We performed finite element (FE) modeling and single-cell RNA sequencing to address this. 4D high-frequency ultrasound imaging of chick embryonic hearts at HH25 (ED 4.5) were obtained for both LAL and control. Motion tracking was performed to quantify strains. Image-based FE modeling was conducted, using the direction of the smallest strain eigenvector as the orientations of contractions, the Guccione active tension model and a Fung-type transversely isotropic passive stiffness model that was determined via micro-pipette aspiration. Single-cell RNA sequencing of left ventricle (LV) heart tissues was performed for normal and LAL embryos at HH30 (ED 6.5) and differentially expressed genes (DEG) were identified.After LAL, LV thickness increased by 33%, strains in the myofiber direction increased by 42%, while stresses in the myofiber direction decreased by 50%. These were likely related to the reduction in ventricular preload and underloading of the LV due to LAL. RNA-seq data revealed potentially related DEG in myocytes, including mechano-sensing genes (Cadherins, NOTCH1, etc.), myosin contractility genes (MLCK, MLCP, etc.), calcium signaling genes (PI3K, PMCA, etc.), and genes related to fibrosis and fibroelastosis (TGF-β, BMP, etc.). We elucidated the changes to the myocardial biomechanics brought by LAL and the corresponding changes to myocyte gene expressions. These data may be useful in identifying the mechanobiological pathways of HLHS.

Indexed as

Atrial FibrillationHypoplastic Left Heart SyndromeBiomechanical PhenomenaHeart AtriaHeart VentriclesHumansMyocardiumBiomechanicsEmbryonic heartHypoplastic left heart syndromeMechanobiologySingle-cell RNA sequencing

Identifiers

PMID37032398
PMCPMC10122626
OpenAlexW4362724215

What OpenQuestion holds

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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.