ArticleCell discovery2023
Lineage-specific regulatory changes in hypertrophic cardiomyopathy unraveled by single-nucleus RNA-seq and spatial transcriptomics.
Article in Cell discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- The molecular and cellular landscape of hypertrophic cardiomyopathy phenotypes: transition from obstructive to end-stage heart failure.Journal of molecular medicine (Berlin, Germany) · 2025Pooled it
- Roles of inflammation and metabolic dysfunction in cardiovascular diseases: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- Vasohibin 1 acts as a key regulator of arrhythmogenesis in pressure-overload-induced cardiac hypertrophy.Acta pharmacologica Sinica · 2026Article
- Immature and mature myocardium in the pathophysiology of hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2026Review
- Phenotypic patterns in feline heart failure: A natural model for understanding variable disease severity in humans.iScience · 2026Article
- Using the simple telegraph model to decipher transcriptional burst regulation across genome-wide data.iScience · 2026Article
- Multiple triggering mechanisms of myocardial fibrosis: Comparison and integration in different disease contexts.iScience · 2026Review
- Targeting RUNX1 protects against diastolic dysfunction in a two-hit mouse model of heart failure with preserved ejection fraction.Cardiovascular research · 2026Article
- A TGF-β1/LEF1/β-catenin/JLP network motif regulates autophagy and tubule injury in renal fibrosis.JCI insight · 2026Article
- Targeting Arrhythmogenic Late Sodium Current by FHF1Circulation research · 2026Article
- Contactin-2 mitigates heart failure and cardiac remodeling via regulation of NUPR1 and ferroptosis.Biology direct · 2026Article
- Mavacamten shows broad benefit in human and mouse models of MYBPC3-related hypertrophic cardiomyopathy.Nature cardiovascular research · 2026Article
- Life-span-dependent transcriptional dynamics of the human heart.Science advances · 2026Article
- Conserved Transcriptional Circuits Regulate Cardiac Fibroblast-Mediated Fibrosis.Circulation research · 2026Article
- A large-scale single-nucleus resource reveals a cardiomyocyte-like fibroblast and stage-specific remodeling across cardiomyopathies.BMC medicine · 2026Article
- Decoding the Cardiac Immune Microenvironment and Fibroblast Crosstalk in Radiotherapy Combined with Immunotherapy-Induced Cardiac Fibrosis Based on Single-Cell Transcriptomic Analysis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Deciphering the cardiac neuron landscape in heart failure patients.PLoS computational biology · 2026Article
- Deletion of Cd248 inJournal of molecular and cellular cardiology plus · 2026Article
- Single-Cell Multi-Omics Profiling of Human Septal Myectomy Tissue: Toward Precision Medicine in Obstructive Hypertrophic Cardiomyopathy.Journal of personalized medicine · 2026Review
- Single cell transcriptomic landscape of adult and pediatric non-ischemic cardiomyopathy.Journal of molecular and cellular cardiology · 2026Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Hypertrophic cardiomyopathy (HCM) is the most common cardiac genetic disorder characterized by cardiomyocyte hypertrophy and cardiac fibrosis. Pathological cardiac remodeling in the myocardium of HCM patients may progress to heart failure. An in-depth elucidation of the lineage-specific changes in pathological cardiac remodeling of HCM is pivotal for the development of therapies to mitigate the progression. Here, we performed single-nucleus RNA-seq of the cardiac tissues from HCM patients or healthy donors and conducted spatial transcriptomic assays on tissue sections from patients. Unbiased clustering of 55,122 nuclei from HCM and healthy conditions revealed 9 cell lineages and 28 clusters. Lineage-specific changes in gene expression, subpopulation composition, and intercellular communication in HCM were discovered through comparative analyses. According to the results of pseudotime ordering, differential expression analysis, and differential regulatory network analysis, potential key genes during the transition towards a failing state of cardiomyocytes such as FGF12, IL31RA, and CREB5 were identified. Transcriptomic dynamics underlying cardiac fibroblast activation were also uncovered, and potential key genes involved in cardiac fibrosis were obtained such as AEBP1, RUNX1, MEOX1, LEF1, and NRXN3. Using the spatial transcriptomic data, spatial activity patterns of the candidate genes, pathways, and subpopulations were confirmed on patient tissue sections. Moreover, we showed experimental evidence that in vitro knockdown of AEBP1 could promote the activation of human cardiac fibroblasts, and overexpression of AEBP1 could attenuate the TGFβ-induced activation. Our study provided a comprehensive analysis of the lineage-specific regulatory changes in HCM, which laid the foundation for targeted drug development in HCM.
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Registered trials
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.