TF-FVIIa PAR2-β-Arrestin Signaling Sustains Organ Dysfunction in Coxsackievirus B3 Infection of Mice

Meike Kespohl; Carl Christoph Goetzke; Nadine Althof; Clara Bredow; Nicolas Kelm; Sandra Pinkert; Thomas Bukur; Valesca Bukur; Kristin Grunz; Dilraj Kaur; Arnd Heuser; Michael Mülleder; Martina Sauter; Karin Klingel; Hartmut Weiler; Nikolaus Berndt; Matthias M. Gaida; Wolfram Ruf; Antje Beling

doi:10.1161/atvbaha.123.320157

Key Points

Activation of protease-activated receptors by coagulation proteases links TF-FVIIa signaling to persistent organ dysfunction in coxsackievirus B3 infection.
Preclinical evaluation in mice indicates that beta-arrestin signaling downstream of PAR2 mediates immune pathology rather than classical G-protein pathways.
Targeting coagulation proteases may attenuate organ dysfunction in viral myocarditis; mouse model results warrant further preclinical validation in vivo.

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Implication

Shows that TF-FVIIa and PAR2 signaling sustained organ dysfunction during Coxsackievirus B3 infection in mice, indicating coagulation proteases regulate innate immune responses.

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Kespohl et al. (2024) studied this question.

synapsesocial.com/papers/68e780ddb6db6435876f46de https://doi.org/10.1161/atvbaha.123.320157

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TF-FVIIa PAR2-β-Arrestin Signaling Sustains Organ Dysfunction in Coxsackievirus B3 Infection of Mice

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TF-FVIIa PAR2-β-Arrestin Signaling Sustains Organ Dysfunction in Coxsackievirus B3 Infection of Mice

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