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Elevated BBLN levels as a cause of heart defects in tetralogy of Fallot

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BBLN, a protein with largely unknown function, was found to be upregulated in damaged hearts of children with tetralogy of Fallot, one of the most frequent congenital heart defects. Transgenic mice and in vitro studies showed that elevated BBLN levels triggered heart damage by activation of the protein CAMK2D.

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Fig. 1: BBLN-induced heart fibrosis and remodeling.

References

  1. Wilson, R., Ross, O. & Griksaitis, M. J. Tetralogy of Fallot. BJA Educ. 19, 362–369 (2019). This review describes the prevalence, major cardiac anomalies and clinical features of TOF.

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This is a summary of: Abd Alla, J. et al. BBLN triggers CAMK2D pathology in mice under cardiac pressure overload and potentially in unrepaired hearts with tetralogy of Fallot. Nat. Cardiovasc. Res. https://doi.org/10.1038/s44161-023-00351-6 (2023).

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Elevated BBLN levels as a cause of heart defects in tetralogy of Fallot. Nat Cardiovasc Res 2, 970–971 (2023). https://doi.org/10.1038/s44161-023-00360-5

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  • DOI: https://doi.org/10.1038/s44161-023-00360-5

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