Evidence map›Paper›PMID 42741796›Full record

ArticleAPL bioengineering2026

Biomechanical stress unmasks a fibroblast-dependent hypercontractile-disarray phenotype in MYBPC3 truncation HCM.

Huanzhu Jiang, Ganesh Malayath, Nongmaithem Debeni Devi, Hsin-Yi Cindy Chou, Yasaman Kargar Gaz Kooh, Jingxuan Guo, Ghiska Ramahdita, Jenna Nguyen, Riya Bhakta, Lavanya Aryan and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in APL bioengineering, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Huanzhu JiangDepartment of Biomedical Engineering, Washington University School of Engineering, St. Louis, Missouri 63130, USA.ORCID https://orcid.org/0000-0002-0781-896X
Ganesh MalayathDepartment of Biomedical Engineering, Washington University School of Engineering, St. Louis, Missouri 63130, USA.ORCID https://orcid.org/0000-0003-3455-7512
Nongmaithem Debeni DeviDepartment of Biomedical Engineering, Washington University School of Engineering, St. Louis, Missouri 63130, USA.ORCID https://orcid.org/0009-0000-8001-9534
Hsin-Yi Cindy ChouDepartment of Biomedical Engineering, Washington University School of Engineering, St. Louis, Missouri 63130, USA.ORCID https://orcid.org/0009-0004-1958-076X
Yasaman Kargar Gaz KoohThe Institute of Materials Science & Engineering, Washington University School of Engineering, St. Louis, Missouri 63130, USA.ORCID https://orcid.org/0009-0005-3257-2921
Jingxuan GuoDepartment of Mechanical Engineering & Materials Science, Washington University School of Engineering, St. Louis, Missouri 63130, USA.ORCID https://orcid.org/0000-0002-3344-2839
Ghiska RamahditaDepartment of Mechanical Engineering & Materials Science, Washington University School of Engineering, St. Louis, Missouri 63130, USA.ORCID https://orcid.org/0000-0002-8587-6954
Jenna NguyenDepartment of Biomedical Engineering, Washington University School of Engineering, St. Louis, Missouri 63130, USA.
Riya BhaktaDepartment of Biomedical Engineering, Washington University School of Engineering, St. Louis, Missouri 63130, USA.
Lavanya AryanDepartment of Biomedical Engineering, Washington University School of Engineering, St. Louis, Missouri 63130, USA.
Sharon CresciCardiovascular Division, Department of Medicine, and Department of Genetics, Washington University School of Medicine, St. Louis, Missouri 63130, USA.ORCID https://orcid.org/0000-0002-5417-1054
Nathaniel HuebschORCID https://orcid.org/0000-0002-3329-0214

Funding

Determining Potential Mechanisms of Worse Outcomes in Black HCM PatientsR01HL170079 · NHLBI · WASHINGTON UNIVERSITY · PI SHARON CRESCI · 2023 to 2026
$3.0M
Biomaterial Platforms to Model the Role of Mechanical Overload in MYBPC3-Linked Hypertrophic CardiomyopathyR01HL159094 · NHLBI · WASHINGTON UNIVERSITY · PI HUEBSCH, NATHANIEL · 2021 to 2025
$2.0M
NHLBI NIH HHS R01 HL159094NHLBI NIH HHS R01 HL170079
6 · The paper itself

Abstract

Hypertrophic cardiomyopathy (HCM) is commonly caused by pathogenic variants in the sarcomere, such as truncations in myosin-binding protein C (MYBPC3), yet clinical severity and adverse outcomes correlate poorly with genotype alone and are strongly influenced by fibrosis. We developed an engineered human micro-heart tissue (

Identifiers

PMID42741796
PMCPMC13574545

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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.