Evidence map›Paper›PMID 35338173›Full record

ArticleScientific reports2022

Altered intercellular communication and extracellular matrix signaling as a potential disease mechanism in human hypertrophic cardiomyopathy.

Amy Larson, Christina J Codden, Gordon S Huggins, Hassan Rastegar, Frederick Y Chen, Barry J Maron, Ethan J Rowin, Martin S Maron, Michael T Chin

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  13. The role of mechanosignaling in the control of myocardial mass.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  14. Single Cell Transcriptomic Profiling ofJournal of the American Heart Association · 2025
    Article
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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 1 institution in 1 country.

Amy Larson *Molecular Cardiology Research Institute, Tufts Medical Center, 800 Washington Street, Box 80, Boston, MA, 02111, USA.
Christina J Codden *Molecular Cardiology Research Institute, Tufts Medical Center, 800 Washington Street, Box 80, Boston, MA, 02111, USA.
Gordon S HugginsMolecular Cardiology Research Institute, Tufts Medical Center, 800 Washington Street, Box 80, Boston, MA, 02111, USA.
Hassan RastegarCardioVascular Center, Tufts Medical Center, Boston, MA, USA.
Frederick Y ChenCardioVascular Center, Tufts Medical Center, Boston, MA, USA.
Barry J MaronCardioVascular Center, Tufts Medical Center, Boston, MA, USA.
Ethan J RowinCardioVascular Center, Tufts Medical Center, Boston, MA, USA.
Martin S MaronCardioVascular Center, Tufts Medical Center, Boston, MA, USA.
Michael T ChinMolecular Cardiology Research Institute, Tufts Medical Center, 800 Washington Street, Box 80, Boston, MA, 02111, USA. mchin3@tuftsmedicalcenter.org.
Tufts Medical Center · US

Funding

Tufts Clinical and Translational Science Institute (Pilot Supplement)UL1TR002544 · NCATS · TUFTS UNIVERSITY BOSTON · PI SELKER, HARRY P. · 2018 to 2022
$50.2M
Characterization of Pathological Pathways of Hypertrophic Cardiomyopathy at Single Cell ResolutionF32HL147492 · NHLBI · TUFTS MEDICAL CENTER · PI GORDON, AMY LARSON · 2020 to 2020
$32k
NCATS NIH HHS UL1 TR002544NHLBI NIH HHS F32 HL147492
6 · The paper itself

Abstract

Hypertrophic cardiomyopathy (HCM) is considered a primary disorder of the sarcomere resulting in unexplained left ventricular hypertrophy but the paradoxical association of nonmyocyte phenotypes such as fibrosis, mitral valve anomalies and microvascular occlusion is unexplained. To understand the interplay between cardiomyocyte and nonmyocyte cell types in human HCM, single nuclei RNA-sequencing was performed on myectomy specimens from HCM patients with left ventricular outflow tract obstruction and control samples from donor hearts free of cardiovascular disease. Clustering analysis based on gene expression patterns identified a total of 34 distinct cell populations, which were classified into 10 different cell types based on marker gene expression. Differential gene expression analysis comparing HCM to Normal datasets revealed differences in sarcomere and extracellular matrix gene expression. Analysis of expressed ligand-receptor pairs across multiple cell types indicated profound alteration in HCM intercellular communication, particularly between cardiomyocytes and fibroblasts, fibroblasts and lymphocytes and involving integrin β1 and its multiple extracellular matrix (ECM) cognate ligands. These findings provide a paradigm for how sarcomere dysfunction is associated with reduced cardiomyocyte secretion of ECM ligands, altered fibroblast ligand-receptor interactions with other cell types and increased fibroblast to lymphocyte signaling, which can further alter the ECM composition and promote nonmyocyte phenotypes.

Indexed as

Cardiomyopathy, HypertrophicCell CommunicationExtracellular MatrixHumansLigandsSarcomeresLigands

Identifiers

PMID35338173
PMCPMC8956620
OpenAlexW4226350863

What OpenQuestion holds

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LicenceCC BY
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.