CaMKIIδ, a calcium/calmodulin-dependent protein kinase, plays pivotal roles in the development of heart disease. In this issue of The Journal of Pathology, Salma Awad and colleagues demonstrate that CaMKIIδ is engaged in both pathological hypertrophy and heart failure. By analysis of mouse and human heart samples, they found that the level of CaMKIIδ is increased in both pathological processes. Further studies demonstrated that CaMKIIδ mediates the phosphorylation of histone H3 at serine 10 (H3S10), which then tethers the chaperone protein 14-3-3 to promoter regions of fetal cardiac genes to activate their transcription. Combined with recent highlights on transcription regulation, this study revealed a fuzzy boundary between pathological hypertrophy and subsequent heart failure and indicates that current therapeutic strategies towards heart failure may have potential risks to patients.
Keywords: CaMKIIδ; heart failure; pathological hypertrophy.
Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.