ArticleScientific reports2022
Tumor endothelial marker 1 is upregulated in heart after cardiac injury and participates in cardiac remodeling.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Expression of tumor endothelial marker 1 in cardiac fibroblast contributes to atrial fibrosis in atrial fibrillation.Scientific reports · 2025Article
- High plasma levels of endosialin and cardiovascular events in patients undergoing coronary angiography.Heart and vessels · 2024Article
- TEM1/endosialin/CD248 promotes pathologic scarring and TGF-β activity through its receptor stability in dermal fibroblasts.Journal of biomedical science · 2024Article
- Regulation of matrix reloading by tumor endothelial marker 1 protects against abdominal aortic aneurysm.International journal of biological sciences · 2024Article
- Soluble tumor endothelial marker 1 in heart failure with reduced ejection fraction: A pilot study.Frontiers in cardiovascular medicine · 2022Article
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Authors and funding
15 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor endothelial marker 1 (TEM1) is a transmembrane glycoprotein that appears on mesenchymal lineage-derived cells during embryogenesis, but its expression greatly reduces after birth. Re-upregulation of TEM1 is found in tumor angiogenesis, organ fibrosis and wound healing indicating its potential role in tissue remodeling and repair. The expression level and function of TEM1 in adult heart are unknown. In explanted hearts from heart failure (HF) patients received cardiac transplantation, immunofluorescence staining showed TEM1 was expressed in cardiomyocytes (CMs) and cardiac fibroblasts. Bioinformatics analysis showed TEM1 upregulation in mouse heart after coronary ligation. Cardiac TEM1 expression was reconfirmed in mouse HF induced by coronary ligation or doxorubicin injection. TEM1 expression increased in cultured CMs stimulated with mechanical stretch, doxorubicin and hypoxia. Further studies showed recombinant TEM1 (rTEM1) was a functional protein that influenced cell behaviors of CMs. It directly activated Erk and Akt through interaction with PDGF receptor. TEM1
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