Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

RhoA Signaling in Immune Cell Response and Cardiac Disease

Version 1 : Received: 3 June 2021 / Approved: 9 June 2021 / Online: 9 June 2021 (21:49:26 CEST)

How to cite: Kilian, L.S.; Frank, D.; Rangrez, A.Y. RhoA Signaling in Immune Cell Response and Cardiac Disease. Preprints 2021, 2021060270 (doi: 10.20944/preprints202106.0270.v1). Kilian, L.S.; Frank, D.; Rangrez, A.Y. RhoA Signaling in Immune Cell Response and Cardiac Disease. Preprints 2021, 2021060270 (doi: 10.20944/preprints202106.0270.v1).

Abstract

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 spirals 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.

Keywords

RhoA; cardiac inflammation; immune cells; cardiocrine signaling; cardiac diseases

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