Key result
RAA-CardAPs reduce fibrosis and improve cardiac function in murine models of CVB3-induced myocarditis.
Why the study?
To overcome limited cell yields from endomyocardial biopsies, researchers isolated CardAPs from human right atrial appendages to evaluate their cardioprotective and immunomodulatory potential in viral myocarditis.
Does intravenous injection of RAA-CardAPs improve cardiac function and reduce fibrosis in murine models of acute and chronic CVB3-induced myocarditis?
Does intravenous injection of RAA-CardAPs improve cardiac function and reduce fibrosis in murine models of acute and chronic CVB3-induced myocarditis?
Human right atrial appendage-derived stromal cells reduce cardiac fibrosis and improve left ventricular function in murine models of acute and chronic viral myocarditis.
Does not support clinical use in viral myocarditis; hypothesis-generating for RAA-CardAP translation to human trials.
We previously have shown the potential of human endomyocardial biopsy (EMB)-derived cardiac adherent proliferating cells (CardAPs) as a new cell-therapeutic treatment option for virus-induced myocarditis. To overcome the limited cell yield per EMB, CardAPs have been isolated from the human right atrial appendage (RAA) in view of allogeneic application and off-the-shelf use. We aimed to investigate the cardioprotective and immunomodulatory potential of RAA-CardAPs in experimental acute and chronic Coxsackievirus B3 (CVB3)-induced myocarditis upon injection in the viral and inflammatory phase. In the acute model, male C57BL6/J mice were intraperitoneally (i.p.) injected with the CVB3 Nancy strain or phosphate buffered saline (PBS). One day after infection, mice were intravenously (i.v.) injected with RAA-CardAPs, EMB-CardAPs (as reference cells) or PBS. For the chronic model, male Naval Medical Research Institute mice were i.p. injected with the CVB3 31-1-93 strain or PBS. Ten days after infection, mice were i.v. injected with RAA-CardAPs. Cardiac function was characterized, followed by harvest of the left ventricle (LV) and spleen for subsequent analysis, 7 and 28 days after CVB3 infection in the acute and chronic model, respectively. In the acute model, RAA-CardAPs decreased cardiac fibrosis and improved cardiac function in CVB3 mice. RAA-CardAPs mice exerted immunomodulatory effects as evidenced by lower LV chemokines expression (C-C motif ligand [CCL]2 and CCL7), CD68+ cells presence, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, tumor necrosis factor-α, and IL-6 mRNA expression. In the chronic model, RAA-CardAPs reduced cardiac fibrosis and the severity of myocarditis, associated with an improvement in LV function. We conclude that RAA-CardAPs represent a treatment strategy to reduce the development of acute and chronic CVB3-induced myocarditis.
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El‐Shafeey et al. (2025) studied Coxsackievirus B3-induced myocarditis. Human right atrial appendage-derived stromal cells (RAA-CardAPs) vs. PBS or EMB-CardAPs was evaluated on Cardiac function, cardiac fibrosis, and immunomodulatory effects. Human right atrial appendage-derived stromal cells (RAA-CardAPs) decreased cardiac fibrosis, improved cardiac function, and exerted immunomodulatory effects in murine models of acute and chronic Coxsackievirus B3-induced myocarditis.
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