Evidence map›Paper›PMID 36237479›Full record

ArticleCardiology and cardiovascular medicine2022

Single Nucleus RNA-sequencing Reveals Altered Intercellular Communication and Dendritic Cell Activation in Nonobstructive Hypertrophic Cardiomyopathy.

Christina J Codden, Amy Larson, Junya Awata, Gayani Perera, Michael T Chin

Open access · hybridAbstract read
In one paragraph

Article in Cardiology and cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
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  7. 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

5 authors at 1 institution in 1 country.

Christina J CoddenMolecular Cardiology Research Institute, Tufts Medical Center, Boston, MA, USA.
Amy LarsonMolecular Cardiology Research Institute, Tufts Medical Center, Boston, MA, USA.
Junya AwataMolecular Cardiology Research Institute, Tufts Medical Center, Boston, MA, USA.
Gayani PereraMolecular Cardiology Research Institute, Tufts Medical Center, Boston, MA, USA.
Michael T ChinMolecular Cardiology Research Institute, Tufts Medical Center, Boston, MA, USA.
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

End stage, nonobstructive hypertrophic cardiomyopathy (HCM) is an intractable condition with no disease-specific therapies. To gain insights into the pathogenesis of nonobstructive HCM, we performed single nucleus RNA-sequencing (snRNA-seq) on human HCM hearts explanted at the time of cardiac transplantation and organ donor hearts serving as controls. Differential gene expression analysis revealed 64 differentially expressed genes linked to specific cell types and molecular functions. Analysis of ligand-receptor pair gene expression to delineate potential intercellular communication revealed significant reductions in expressed ligand-receptor pairs likely affecting the extracellular matrix, growth factor binding, peptidase regulator activity, platelet-derived growth factor binding and protease binding in the HCM tissue. Changes in Integrin-β1 receptor expression were responsible for many observed changes related to extracellular matrix interactions, by increasing in dendritic, smooth muscle and pericyte cells while decreasing in endothelial and fibroblast cells, suggesting potential mechanisms for fibrosis and microvascular disease in HCM and a potential role for dendritic cells. In contrast, there was an increase in ligand-receptor pair expression associated with adenylate cyclase binding, calcium channel molecular functions, channel inhibitor activity, ion channel inhibitor activity, phosphatase activator activity, protein kinase activator activity and titin binding, suggesting important shifts in various signaling cascades in nonobstructive, end stage HCM.

Identifiers

PMID36237479
PMCPMC9555339
OpenAlexW4293408689

What OpenQuestion holds

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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.