RhoA signaling in immune cell response and cardiac disease
Chronic inflammation, the activation of immune cells and their cross-talk with cardiomyocytes in the pathogenesis and progression of heart diseases has long been overlooked. However, with the latest research developments, it is increasingly accepted that a vicious cycle exists where cardiomyocytes r...
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| Main Authors: | , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
3 July 2021
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| In: |
Cells
Year: 2021, Volume: 10, Issue: 7, Pages: 1-15 |
| ISSN: | 2073-4409 |
| DOI: | 10.3390/cells10071681 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.3390/cells10071681 Verlag, lizenzpflichtig, Volltext: https://www.mdpi.com/2073-4409/10/7/1681 |
| Author Notes: | by Lucia Sophie Kilian, Derk Frank and Ashraf Yusuf Rangrez |
| Summary: | Chronic inflammation, the activation of immune cells and their cross-talk with cardiomyocytes in the pathogenesis and progression of heart diseases has long been overlooked. However, with the latest research developments, it is increasingly accepted that a vicious cycle exists where cardiomyocytes release cardiocrine signaling molecules that spiral down to immune cell activation and chronic state of low-level inflammation. For example, cardiocrine molecules released from injured or stressed cardiomyocytes can stimulate macrophages, dendritic cells, neutrophils and even T-cells, which then subsequently increase cardiac inflammation by co-stimulation and positive feedback loops. One of the key proteins involved in stress-mediated cardiomyocyte signal transduction is a small GTPase RhoA. Importantly, the regulation of RhoA activation is critical for effective immune cell response and is being considered as one of the potential therapeutic targets in many immune-cell-mediated inflammatory diseases. In this review we provide an update on the role of RhoA at the juncture of immune cell activation, inflammation and cardiac disease. |
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| Item Description: | Gesehen am 29.09.2021 |
| Physical Description: | Online Resource |
| ISSN: | 2073-4409 |
| DOI: | 10.3390/cells10071681 |