Evidence map›Paper›PMID 40750715›Full record

ReviewNature protocols2026

Modeling heart rhythm using human engineered heart tissues.

Chengyi Tu, Arianne Caudal, Yu Liu, Sanjiv M Narayan, Joseph C Wu

Abstract readReview
In one paragraph

Review in Nature protocols, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

5 authors.

Chengyi TuStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA. cytu@stanford.edu.
Arianne CaudalStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.ORCID 0000-0001-9836-9436
Yu LiuStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.
Sanjiv M NarayanStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.
Joseph C WuStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA. joewu@stanford.edu.ORCID 0000-0002-6068-8041

Funding

Human Induced Pluripotent Stem Cells for Cardiovascular Disease ModelingR01HL113006 · NHLBI · STANFORD UNIVERSITY · PI WU, JOSEPH C. · 2012 to 2025
$6.8M
Human iPSCs for Elucidating Intercellular Crosstalk Signaling in Dilated CardiomyopathyR01HL141371 · NHLBI · STANFORD UNIVERSITY · PI WONG, WING H., WU, JOSEPH C. · 2018 to 2025
$6.2M
Modeling Tyrosine Kinase Inhibitor-Induced Vascular Dysfunction Using Human iPSCsR01HL141851 · NHLBI · STANFORD UNIVERSITY · PI WONG, WING H., WU, JOSEPH C. · 2018 to 2025
$5.7M
Machine Learning for Ventricular ArrhythmiasR01HL162260 · NHLBI · STANFORD UNIVERSITY · PI Sanjiv M Narayan · 2023 to 2026
$2.5M
Elucidating ECM Signaling in Cardiac Organoids with Machine Learning and Single-cell MultiomicsR01HL163680 · NHLBI · STANFORD UNIVERSITY · PI RAJADAS, JAYAKUMAR, WONG, WING H. · 2022 to 2025
$2.5M
Tachycardia-induced Metabolic Remodeling Drives Cardiac DysfunctionK99HL164962 · NHLBI · STANFORD UNIVERSITY · PI TU, CHENGYI · 2023 to 2024
$303k
American Heart Association (American Heart Association, Inc.) 908136NHLBI NIH HHS K99 HL164962NHLBI NIH HHS R01 HL113006NHLBI NIH HHS R01 HL141371NHLBI NIH HHS R01 HL141851NHLBI NIH HHS R01 HL162260NHLBI NIH HHS R01 HL163680
6 · The paper itself

Abstract

Heart rate is both an indicator and modulator of cardiovascular health. Prolonged elevation in heart rate or irregular heart rhythm can trigger the onset of cardiac dysfunction, a condition termed 'tachycardia-induced cardiomyopathy'. While large animals have historically served as the primary model for studying this condition owing to their similar resting heart rates to humans, their use is limited by cost and throughput constraints. We recently developed the first engineered model of tachycardia-induced cardiomyopathy to overcome this technical bottleneck. Our model uses matured human engineered myocardium coupled with programmable electrical stimulation to emulate the pathophysiological changes in human heart rhythm. This in vitro model, capable of acutely and chronically modulating both beating rate and rhythm, recapitulated the clinical hallmarks of tachycardia-induced cardiomyopathy, and its utility was further validated via molecular comparisons against data from a canine model and human patients. Moreover, this model has improved the throughput and relevance to human genetics, enabling deep mechanistic explorations that were previously impossible. Here we present a comprehensive workflow detailing the fabrication and maturation of human engineered heart tissue, assembly of the electrical pacing system, functional analysis using open-source software and preparation for proteomic and transcriptomic analyses. This 5-week Protocol could be implemented by an experienced bench scientist with strong expertise in cell culture, ideally involving stem cell-derived cardiomyocytes. Given the broad implications of heart rhythm alterations in various cardiac conditions, this workflow can be employed with other biophysical and chemical cues to generate more complex and physiologically relevant cardiac models.

Indexed as

HeartHeart RateModels, CardiovascularTissue EngineeringAnimalsCardiomyopathiesDogsHumansMyocardiumMyocytes, Cardiac

Identifiers

PMID40750715
PMCPMC13132113

What Socratic 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 Socratic graph.