The DOI matches its Crossref record; 67 of the 68 references it cites were found in a registry or an index.
Cell-cell interaction in the heart via Wnt/ -catenin pathway after cardiac injury
Open accessAbstract
The adult mammalian heart predominantly comprises myocytes, fibroblasts, endothelial cells, smooth muscle cells, and epicardial cells arranged in a precise three-dimensional framework. Following cardiac injury, the spatial arrangement of cells is disrupted as different populations of cells are recruited to the heart in a temporally regulated manner. The alteration of the cellular composition of the heart after cardiac injury thus enables different phenotypes of cells to interact with each other in a spatio-temporal-dependent manner. It can be argued that the integrated study of such cellular interactions rather than the examination of single populations of cells can provide more insights into the biology of cardiac repair especially at an organ-wide level. Many signalling systems undoubtedly mediate such cross talk between cells after cardiac injury. The Wnt/β-catenin system plays an important role during cardiac development and disease. Here, we describe how cell populations in the heart after cardiac injury mediate their interactions via the Wnt/β-catenin pathway, determine how such interactions can affect a cardiac repair response and finally suggest an integrated approach to study cardiac cellular interactions.
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“Cardiac pathophysiology often arises from interactions between CMs, fibroblasts (FBs), endothelial cells, smooth muscle cells, and other supporting cell types (Deb, 2014; Tan et al., 2024).”
From Mini-hearts for disease modeling and drug testing – process optimization versus biological functionality (2026) · cites this paper as Deb, 2014
In the citing paper
“However, restricting models to only CMs and FBs may overlook crucial cell interactions in diseases like myocardial infarction (Deb, 2014; Tan et al., 2024).”
From Mini-hearts for disease modeling and drug testing – process optimization versus biological functionality (2026) · cites this paper as Deb, 2014
Citations
Cites
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p53-induced inhibition of Hif-1 causes cardiac dysfunction during pressure overload
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Research works printed but not linked: 1
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Cited by
Items 101–104 of 104
Wang, J., Xia, Y., Lu, A., Wang, H., Davis, D. R., Liu, P. X., Beanlands, R. S., & Liang, W. (2021) · Research Square · doi:10.21203/rs.3.rs-393358/v2
Morpho-functional impact of Vangl2 on hippocampus development
Carvalho, S. D. S. (2016) · theses.fr (ABES) · doi:10.70675/cfbdb0fezf7c3z4a06zb785zeaefd18084a9
Zhi, M., Wang, A., Quan, H., & Hong, L. (2026) · Chinese Herbal Medicines · doi:10.1016/j.chmed.2026.05.014
Cardiac regeneration and repair: the emerging mechanisms and therapeutic approaches
Li, Y., Zheng, K., Liu, Y., Li, R., Wang, S., Ye, W., Luo, Z., Li, X., Tao, Z., Xia, J., et al. (2026) · Molecular Biomedicine · doi:10.1186/s43556-026-00504-6
Metadata
- Authors
- Deb, A.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Deb, A.
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2014-03-03
- Volume
- 102
- Issue
- 2
- Pages
- 214-223
- ISSN
- 0008-6363 (ISSN-L)
- PMC
- PMC3989450
- OpenAlex
- W2120472949
- Cited by
- 102
- References
- 68
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 6 · 2023: 3 · 2022: 5 · 2021: 13 · 2020: 10 · 2019: 12 · 2018: 7 · 2017: 14 · 2016: 11 · 2015: 6 · 2014: 4
- FWCI
- 1.10
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cardiovascular Research (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL102190)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Keywords
- Wnt/β-catenin signaling, cell-cell interactions, cardiac injury, cardiac repair, cardiac fibroblasts, epicardial cells, endothelial cells, smooth muscle cells, cardiomyocytes
- MeSH terms
- Animals, Cell Communication, Heart, Heart Injuries, Humans, Signal Transduction, beta Catenin, Wnt Signaling Pathway
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
