Ventricular arrhythmias are associated with aging and are a leading cause of sudden cardiac death. A new study shows that hyperactivation of p38γ/δ MAPKs is a key driver of stress-induced ventricular arrhythmias via increased phosphorylation of ryanodine receptor 2 at Ser2367 and impaired localization of potassium voltage-gated channel Kv4.3.
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Acknowledgements
This work was supported by the Robert and Janice McNair foundation (J.A.K.), and NIH R01-HL089598, R01-HL147108, R01-HL153350 and R01-HL160992 (X.H.T.W.).
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X.H.T.W. is a founding partner of Elex Biotech, a start-up company that develops drug molecules that target ryanodine receptors to treat cardiac arrhythmias. X.H.T.W. is also a consultant to Rocket Pharmaceuticals. J.A.K. declares no competing interests.
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Keefe, J.A., Wehrens, X.H.T. Blocking p38γ/δ, a molecular cardiac defibrillator. Nat Cardiovasc Res 2, 1104–1106 (2023). https://doi.org/10.1038/s44161-023-00363-2
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DOI: https://doi.org/10.1038/s44161-023-00363-2