ArticleNature cardiovascular research2022
A human cell atlas of the pressure-induced hypertrophic heart.
Article in Nature cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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.
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.
Who cites it
40 citing papers in PubMed.
- Leptin Receptor Fibroblasts Are Preferential Contributors to Cardiac Fibrosis.Circulation research · 2026Article
- Endothelial ZBTB16: a molecular shield against cardiac aging.European heart journal · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- High-Throughput Cardiac Hypertrophy Phenotyping Supports Lead Optimization of GRK5 Inhibitors.ACS medicinal chemistry letters · 2026Article
- Leveraging Single-Cell Technologies to Advance Understanding of Myocardial Disease.Circulation research · 2026Review
- DoTools: a cross platform framework to streamline common single cell workflows.Bioinformatics advances · 2026Article
- Decoding heart failure subtypes with neural networks via differential explanation analysis.Briefings in bioinformatics · 2025Article
- A cross-study transcriptional patient map of heart failure defines conserved multicellular coordination in cardiac remodeling.Nature communications · 2025Article
- Modeling myocardial physiological growth using human pluripotent stem cell derived cardiomyocytes and 3D cardiac microtissues.Cellular and molecular life sciences : CMLS · 2025Article
- Beneficial effects of vascular endothelial growth factor B gene transfer in the aged heart.Cardiovascular research · 2025Article
- Integrated multiomics of pressure overload in the human heart prioritizes targets relevant to heart failure.Nature communications · 2025Article
- Targeting miRNA-1a and miRNA-15b: A Novel Combinatorial Strategy to Drive Adult Cardiac Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- ARID5A orchestrates cardiac aging and inflammation through MAVS mRNA stabilization.Nature cardiovascular research · 2025Article
- Cardiac Fibrosis in the Multi-Omics Era: Implications for Heart Failure.Circulation research · 2025Review
- The cellular and molecular cardiac tissue responses in human inflammatory cardiomyopathies after SARS-CoV-2 infection and COVID-19 vaccination.Nature cardiovascular research · 2025Article
- The role of mechanosignaling in the control of myocardial mass.American journal of physiology. Heart and circulatory physiology · 2025Review
- Nsun2 controls cardiac homeostasis and hypertrophic response by regulating PRKACA expression.Theranostics · 2025Article
- Genome-wide association analysis provides insights into the molecular etiology of dilated cardiomyopathy.Nature genetics · 2024Article
- Beyond the Heartbeat: Single-Cell Omics Redefining Cardiovascular Research.Current cardiology reports · 2024Review
- Single-Cell RNA Sequencing and Combinatorial Approaches for Understanding Heart Biology and Disease.Biology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pathological cardiac hypertrophy is a leading cause of heart failure, but knowledge of the full repertoire of cardiac cells and their gene expression profiles in the human hypertrophic heart is missing. Here, by using large-scale single-nucleus transcriptomics, we present the transcriptional response of human cardiomyocytes to pressure overload caused by aortic valve stenosis and describe major alterations in cardiac cellular crosstalk. Hypertrophied cardiomyocytes had reduced input from endothelial cells and fibroblasts. Genes encoding Eph receptor tyrosine kinases, particularly EPHB1, were significantly downregulated in cardiomyocytes of the hypertrophied heart. Consequently, EPHB1 activation by its ligand ephrin (EFN)B2, which is mainly expressed by endothelial cells, was reduced. EFNB2 inhibited cardiomyocyte hypertrophy in vitro, while silencing its expression in endothelial cells induced hypertrophy in co-cultured cardiomyocytes. Our human cell atlas of the hypertrophied heart highlights the importance of intercellular crosstalk in disease pathogenesis and provides a valuable resource.
Identifiers
What Socratic holds
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 Socratic graph.