ArticleScientific reports2016
Crim1 has cell-autonomous and paracrine roles during embryonic heart development.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Cytokine-associated ROS and Ca2+ dysregulation in severe inflammatory cardiomyopathy.Cardiovascular research · 2026Observational
- Plasma Proteomics Reveals Dysregulated Pathways Across the SpectrumCirculation. Genomic and precision medicine · 2025Article
- Epicardium-myocardium crosstalk orchestrates heart development.Frontiers in cell and developmental biology · 2025Review
- Single-cell multi-omics analysis reveals cellular subpopulations associated with relapse in high-risk B-ALL following intensified chemotherapy.Frontiers in immunology · 2025Article
- Prognostic Significance of Proteomics-Discovered Circulating Inflammatory Biomarkers in Patients With Pulmonary Arterial Hypertension.Journal of the American Heart Association · 2024Article
- Crim1 inhibits angiotensin II-induced hypertrophy and preserves Kv4.2 expression in cardiomyocytes.Iranian journal of basic medical sciences · 2022Article
- The TFEB-TGIF1 axis regulates EMT in mouse epicardial cells.Nature communications · 2022Article
- Skeletal muscle transcriptome in healthy aging.Nature communications · 2021Article
- Crim1 suppresses left ventricular hypertrophy.Biomedical reports · 2019Article
- CRIM1 is necessary for coronary vascular endothelial cell development and homeostasis.Journal of molecular histology · 2017Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epicardium has a critical role during embryonic development, contributing epicardium-derived lineages to the heart, as well as providing regulatory and trophic signals necessary for myocardial development. Crim1 is a unique trans-membrane protein expressed by epicardial and epicardially-derived cells but its role in cardiogenesis is unknown. Using knockout mouse models, we observe that loss of Crim1 leads to congenital heart defects including epicardial defects and hypoplastic ventricular compact myocardium. Epicardium-restricted deletion of Crim1 results in increased epithelial-to-mesenchymal transition and invasion of the myocardium in vivo, and an increased migration of primary epicardial cells. Furthermore, Crim1 appears to be necessary for the proliferation of epicardium-derived cells (EPDCs) and for their subsequent differentiation into cardiac fibroblasts. It is also required for normal levels of cardiomyocyte proliferation and apoptosis, consistent with a role in regulating epicardium-derived trophic factors that act on the myocardium. Mechanistically, Crim1 may also modulate key developmentally expressed growth factors such as TGFβs, as changes in the downstream effectors phospho-SMAD2 and phospho-ERK1/2 are observed in the absence of Crim1. Collectively, our data demonstrates that Crim1 is essential for cell-autonomous and paracrine aspects of heart development.
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