Evidence map›Paper›PMID 36902152›Full record

ArticleInternational journal of molecular sciences2023

Multi-Omics Profiling of Hypertrophic Cardiomyopathy Reveals Altered Mechanisms in Mitochondrial Dynamics and Excitation-Contraction Coupling.

Jarrod Moore, Jourdan Ewoldt, Gabriela Venturini, Alexandre C Pereira, Kallyandra Padilha, Matthew Lawton, Weiwei Lin, Raghuveera Goel, Ivan Luptak, Valentina Perissi and 5 more

Open access · goldFull text read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
5.5field-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

14 citing papers in PubMed, 25 citations in OpenAlex.

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  6. Mechano-energetic uncoupling in heart failure.Nature reviews. Cardiology · 2025
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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

15 authors at 5 institutions in 2 countries.

Jarrod MooreCenter for Network Systems Biology, Department of Biochemistry, Boston University School of Medicine, Boston, MA 02118, USA.
Jourdan EwoldtDepartment of Biomedical Engineering, Boston University, Boston, MA 02218, USA.
Gabriela VenturiniDepartment of Genetics, Harvard Medical School, Boston, MA 02115, USA.ORCID 0000-0003-2913-2296
Alexandre C PereiraDepartment of Genetics, Harvard Medical School, Boston, MA 02115, USA.
Kallyandra PadilhaLaboratory of Genetics and Molecular Cardiology, Clinical Hospital, Faculty of Medicine, University of São Paulo, Sao Paulo 05508-000, Brazil.ORCID 0000-0002-7349-4051
Matthew LawtonCenter for Network Systems Biology, Department of Biochemistry, Boston University School of Medicine, Boston, MA 02118, USA.ORCID 0000-0002-7244-1337
Weiwei LinCenter for Network Systems Biology, Department of Biochemistry, Boston University School of Medicine, Boston, MA 02118, USA.
Raghuveera GoelCenter for Network Systems Biology, Department of Biochemistry, Boston University School of Medicine, Boston, MA 02118, USA.
Ivan LuptakMyocardial Biology Unit, Boston University School of Medicine, Boston, MA 02118, USA.ORCID 0000-0001-7498-7694
Valentina PerissiCenter for Network Systems Biology, Department of Biochemistry, Boston University School of Medicine, Boston, MA 02118, USA.
Christine E SeidmanDepartment of Genetics, Harvard Medical School, Boston, MA 02115, USA.
Jonathan SeidmanDepartment of Genetics, Harvard Medical School, Boston, MA 02115, USA.
Michael T ChinMolecular Cardiology Research Institute, Tufts Medical Center, Boston, MA 02145, USA.ORCID 0000-0003-3065-8498
Christopher ChenDepartment of Biomedical Engineering, Boston University, Boston, MA 02218, USA.
Andrew EmiliCenter for Network Systems Biology, Department of Biochemistry, Boston University School of Medicine, Boston, MA 02118, USA.ORCID 0000-0001-8995-246X
Boston University · USHarvard University · USBrigham and Women's Hospital · USTufts Medical Center · USUniversidade de São Paulo · BR

Funding

Defining Pathways from Gene Mutation to Heart FailureR01HL080494 · NHLBI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI CHEN, CHRISTOPHER S, SEIDMAN, CHRISTINE E · 2005 to 2024
$9.4M
Molecular Signaling in Hypertrophic CardiomyopathyR01HL084553 · NHLBI · HARVARD MEDICAL SCHOOL · PI SEIDMAN, JONATHAN G · 2007 to 2022
$5.9M
Regulation of mitochondrial homeostasis through retrograde signalingR01GM127625 · NIGMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI PERISSI, VALENTINA · 2018 to 2021
$1.8M
Targeting Energetics to Improve Outcomes in Hypertrophic CardiomyopathyR56HL157367 · NHLBI · BOSTON MEDICAL CENTER · PI LUPTAK, IVAN · 2022 to 2022
$818k
Hypertrophic cardiomyopathy-induced paracrine signaling and stromal activationF31HL158195 · NHLBI · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI EWOLDT, JOURDAN · 2021 to 2023
$101k
NHLBI NIH HHS F31 HL158195NHLBI NIH HHS R01 HL080494NHLBI NIH HHS R01 HL084553NHLBI NIH HHS R56 HL157367NIGMS NIH HHS R01 GM127625
6 · The paper itself

Abstract

Hypertrophic cardiomyopathy is one of the most common inherited cardiomyopathies and a leading cause of sudden cardiac death in young adults. Despite profound insights into the genetics, there is imperfect correlation between mutation and clinical prognosis, suggesting complex molecular cascades driving pathogenesis. To investigate this, we performed an integrated quantitative multi-omics (proteomic, phosphoproteomic, and metabolomic) analysis to illuminate the early and direct consequences of mutations in myosin heavy chain in engineered human induced pluripotent stem-cell-derived cardiomyocytes relative to late-stage disease using patient myectomies. We captured hundreds of differential features, which map to distinct molecular mechanisms modulating mitochondrial homeostasis at the earliest stages of pathobiology, as well as stage-specific metabolic and excitation-coupling maladaptation. Collectively, this study fills in gaps from previous studies by expanding knowledge of the initial responses to mutations that protect cells against the early stress prior to contractile dysfunction and overt disease.

Indexed as

Cardiomyopathy, HypertrophicInduced Pluripotent Stem CellsHumansMitochondrial DynamicsMultiomicsMutationMyocytes, CardiacProteomicsYoung Adulthuman induced pluripotent stem-cell-derived cardiomyocyteshypertrophic cardiomyopathyliquid chromatography–tandem mass spectrometrymetabolomicsmyectomynetwork systems biologyphosphoproteomics

Identifiers

PMID36902152
PMCPMC10002553
OpenAlexW4322743027

What OpenQuestion holds

Textfull text, public
LicenceCC BY
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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.