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: Kilian, Lucia Sophie (Author) , Frank, Derk (Author) , Rangrez, Ashraf Yusuf (Author)
Format: Article (Journal)
Language:English
Published: 3 July 2021
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
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Author Notes:by Lucia Sophie Kilian, Derk Frank and Ashraf Yusuf Rangrez

MARC

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520 |a 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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