ArticleiScience2022
Analysis of myocardial cellular gene expression during pressure overload reveals matrix based functional intercellular communication.
Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- Left ventricular chamber stiffness and strain determines the myocardial transcriptional response to elevated filling pressure.American journal of physiology. Heart and circulatory physiology · 2026Article
- Spatial imprints of emergent cardiomyocyte states in the pressure-overloaded heart.bioRxiv : the preprint server for biology · 2026Article
- Cardiomyocyte-derived TGFB3 attenuates cardiac fibrosis and preserves cardiac function in heart failure.Scientific reports · 2026Article
- Nonmuscle α-Actinin-4 Couples Sarcomere Function to Cardiac Remodeling.Circulation research · 2026Article
- Downregulation of TCF19 and ATAD2 causes endothelial cell cycle arrest at the transition from cardiac hypertrophy to heart failure.Basic research in cardiology · 2025Article
- Macrophage-Derived CCL24 Promotes Cardiac Fibrosis Via Fibroblast CCR3.Circulation research · 2025Article
- Capillary Endothelial Cells as Therapeutic Target in Pressure Overload-Induced Heart Failure.JACC. Basic to translational science · 2025Article
- Pericardial adipose tissue promotes transition to heart failure with reduced ejection fraction upon pressure-overload in mice.Basic research in cardiology · 2025Article
- Septin4 Regulates Cardiac Fibrosis After Pressure Overload.Circulation research · 2025Article
- The cardiac phospho-proteome during pressure overload in mice.Scientific data · 2025Article
- Asb10 accelerates pathological cardiac remodeling by stabilizing HSP70.Cell death & disease · 2025Article
- Induction of cardiac fibulin-4 protects against pressure overload-induced cardiac hypertrophy and heart failure.Communications biology · 2025Article
- Vitamin A deficiency attenuates cardiac rupture inFrontiers in cardiovascular medicine · 2025Article
- Endothelial derived, secreted long non-coding RNAsMolecular therapy. Nucleic acids · 2024Article
- Transverse aortic constriction multi-omics analysis uncovers pathophysiological cardiac molecular mechanisms.Database : the journal of biological databases and curation · 2024Article
- Treatment with αvβ3-integrin-specific 29P attenuates pressure-overload induced cardiac remodelling after transverse aortic constriction in mice.Journal of molecular and cellular cardiology plus · 2024Article
- Atlas of cardiac endothelial cell enhancer elements linking the mineralocorticoid receptor to pathological gene expression.Science advances · 2024Article
- Inter- and Intracellular Signaling Pathways.Advances in experimental medicine and biology · 2024Review
- Protein Restriction Effects on Healthspan and Lifespan in Drosophila melanogaster Are Additive With a Longevity-Promoting Diet.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023Article
Corrections and comments
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Authors and funding
24 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To identify cellular mechanisms responsible for pressure overload triggered heart failure, we isolated cardiomyocytes, endothelial cells, and fibroblasts as most abundant cell types from mouse hearts in the subacute and chronic stages after transverse aortic constriction (TAC) and performed RNA-sequencing. We detected highly cell-type specific transcriptional responses with characteristic time courses and active intercellular communication. Cardiomyocytes after TAC exerted an early and sustained upregulation of inflammatory and matrix genes and a concomitant suppression of metabolic and ion channel genes. Fibroblasts, in contrast, showed transient early upregulation of inflammatory and matrix genes and downregulation of angiogenesis genes, but sustained induction of cell cycle and ion channel genes during TAC. Endothelial cells transiently induced cell cycle and extracellular matrix genes early after TAC, but exerted a long-lasting upregulation of inflammatory genes. As we found that matrix production by multiple cell types triggers pathological cellular responses, it might serve as a future therapeutic target.
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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.