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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
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Ruegsegger, G. N., Toedebusch, R. G., Braselton, J. F., Childs, T. E., & Booth, F. W. (2016) · Physiological Genomics · doi:10.1152/physiolgenomics.00083.2016 · Cited by 2
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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).”
Decoding the complex genetic causes of heart diseases using systems biology
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Waas, M., Farris, S. D., Kropp, E. M., Beckman, J. A., Stempien‐Otero, A., Mahr, C., & Gundry, R. L. (2016) · Springer eBooks · doi:10.1007/978-3-319-31828-8_6
Innovative reporter gene imaging techniques making inroads to biology
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Vachhani, K. (2016) · TSpace (University of Toronto)
G-baToN: a versatile reporter system for cancer cell-stromal cell interactionsPreprint
Tang, R., Murray, C. W., Linde, I. L., Kramer, N. J., Lyu, Z., Tsai, M. K., Chen, L. C., Cai, H., Gitler, A. D., Engleman, E. G., et al. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.02.01.929877
Ying, L. I., Fang, W. A. N. G., Xiaolong, G. A. O., Zhu, L., Wen, W. A. N. G., & Sharshov, K. (2021) · Kafkas Universitesi Veteriner Fakultesi Dergisi · doi:10.9775/kvfd.2020.25704
Wnt/β-Catenin Signalling Inhibits T-Type Calcium Channels in Cardiomyocytes
Florczak, K. (2021) · uO Research (University of Ottawa) · doi:10.20381/ruor-26205
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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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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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Data sources
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.
