ArticleNature communications2025
Integrated multiomics of pressure overload in the human heart prioritizes targets relevant to heart failure.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Paediatric proteomic signatures of cardiometabolic disease-associated traits predict adult disease outcomes.Nature metabolism · 2026Article
- Proteogenomic Analysis of Coronary Artery Calcification in Human Populations.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Characteristics, clinical outcomes and molecular mechanisms associated with severe diastolic dysfunction in aortic stenosis.Journal of molecular and cellular cardiology plus · 2026Article
- Heterogeneous Myocardial Adaptation to Pressure Overload Reveals a Spared, Vulnerable Segment Identified by Multiparametric Cardiac MRI.NMR in biomedicine · 2026Article
- The Advances in Novel Delivery Strategies for Hirudin Against Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Leveraging Single-Cell Technologies to Advance Understanding of Myocardial Disease.Circulation research · 2026Review
- Disulfidptosis in heart failure: an emerging mechanism awaiting exploration.Frontiers in cardiovascular medicine · 2026Review
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31 authors.
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Abstract
Pressure overload initiates a series of alterations in the human heart that predate macroscopic organ-level remodeling and downstream heart failure. We study aortic stenosis through integrated proteomic, tissue transcriptomic, and genetic methods to prioritize targets causal in human heart failure. First, we identify the circulating proteome of cardiac remodeling in aortic stenosis, specifying known and previously-unknown mediators of fibrosis, hypertrophy, and oxidative stress, several associated with interstitial fibrosis in a separate cohort (N = 145). These signatures are strongly related to clinical outcomes in aortic stenosis (N = 802) and in broader at-risk populations in the UK Biobank (N = 36,668). We next map this remodeling proteome to myocardial transcription in patients with and without aortic stenosis through single-nuclear transcriptomics, observing broad differential expression of genes encoding this remodeling proteome, featuring fibrosis pathways and metabolic-inflammatory signaling. Finally, integrating our circulating and tissue-specific results with modern genetic approaches, we implicate several targets as causal in heart failure.
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