ArticleEuropean heart journal2025
Spatial transcriptional landscape of human heart failure.
Article in European heart journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
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Who cites it
15 citing papers in PubMed.
- Orchestrating glucose metabolism: PFKFB2 as a signal-integrating conductor in homeostasis and disease.The Journal of biological chemistry · 2026Review
- Review
- Traditional Chinese Medicine Intervention Based on Metabolic-Epigenetic Axis: Mechanism and Treatment Strategy of Chronic Heart Failure.Biomolecules · 2026Review
- Imaging-anchored multiomics in cardiovascular disease: integrating cardiac imaging, bulk, single-cell, and spatial transcriptomics.Briefings in bioinformatics · 2026Review
- Myocardial Immune Niches in Homeostasis and Inflammation.Immunological reviews · 2026Review
- Molecular Mechanisms and Multi-Omics Integration in Heart Failure: From Pathophysiology to Precision Medicine.International journal of molecular sciences · 2026Review
- From automation to agentic artificial intelligence in laboratory medicine: an opinion of the IFCC Division on Emerging Technologies.Clinical chemistry and laboratory medicine · 2026Review
- Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Cardiomyocyte-derived TGFB3 attenuates cardiac fibrosis and preserves cardiac function in heart failure.Scientific reports · 2026Article
- From Single Genes to Systemic Networks: Transcriptomic Insights into Traditional Chinese Medicine for Heart Failure.Drug design, development and therapy · 2026Review
- Hypoxia-driven crosstalk among cardiac fibroblasts, macrophages, and endothelial cells in cardiac fibrosis.Frontiers in cell and developmental biology · 2026Review
- Decoding cardiac homeostasis and injury: the evolving landscape of spatial transcriptomics.Frontiers in cell and developmental biology · 2026Review
- Identification of PANoptosis-Related Biomarkers in Hypertrophic Cardiomyopathy: Insights from Multi-Omics Analysis.Journal of inflammation research · 2026Article
- Unravelling heart failure cellular signalling heterogeneity with spatial transcriptomics.European heart journal · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
BACKGROUND AND
aimsHeart failure (HF) remains a significant clinical challenge due to its diverse aetiologies and complex pathophysiology. The molecular alterations specific to distinct cell types and histological patterns during HF progression are still poorly characterized. This study aimed to explore cell-type- and histology-specific gene expression profiles in cardiomyopathies.
methodsNinety tissue cores from 44 participants, encompassing various forms of cardiomyopathy and control samples with diverse histological features, were analysed using the GeoMx Whole Human Transcriptome Atlas. Data on cell types, clinical information, and histological features were integrated to examine gene expression profiles in cardiomyopathy.
resultsThe study characterized the cellular composition of ventricular myocardium and validated the GeoMx platform's efficiency in compartmentalizing specific cell types, demonstrating high accuracy for cardiomyocytes but limitations for endothelial cells and fibroblasts. Differentially expressed genes, including UCHL1 from cardiomyocytes, were associated with degeneration, while CCL14, ACKR1, and PLVAP from endothelial cells were linked to fibrosis. Multiplex immunohistochemistry and integrative analysis of prior sc/snRNA-seq data identified a PLVAP, ACKR1, and CCL14-positive pro-inflammatory endothelial cell subtype linked to fibrosis in HF. Downregulation of ribosomal proteins in cardiomyocytes was associated with myocyte disarray in hypertrophic cardiomyopathy. Additionally, pronounced inflammatory responses were observed in end-stage HF. Combined histological and clinical analysis identified CRIP3, PFKFB2, and TAX1BP3 as novel contributors to HF pathogenesis.
conclusionsThese findings highlight the critical role of cell-enriched and histology-specific transcriptome mapping in understanding the complex pathophysiological landscape of failing hearts, offering molecular insights and potential therapeutic targets for future interventions.
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