As a subunit of the calcium/calmodulin dependent protein kinase II complex, calcium/calmodulin dependent protein kinase II complex δ (CAMK2D) modulates the functions of ion channels and Ca2+ handling proteins. It also regulates the phosphorylation and acetylation of histones. It has been shown to be overexpressed in the myocardium of diabetic patients.
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The Journal of pathology, 235(4), 606-618 (2014-11-26)
Heart failure is associated with the reactivation of a fetal cardiac gene programme that has become a hallmark of cardiac hypertrophy and maladaptive ventricular remodelling, yet the mechanisms that regulate this transcriptional reprogramming are not fully understood. Using mice with
Diabetes mellitus (DM) is an increasing epidemic that places a significant burden on health services worldwide. The incidence of heart failure (HF) is significantly higher in diabetic patients compared to non-diabetic patients. One underlying mechanism proposed for the link between
Heart failure (HF) is known to be associated with increased Ca(2+)/calmodulin-dependent protein kinase (CaMK)II expression and activity. There is still controversial discussion about the functional role of CaMKII in HF. Moreover, CaMKII inhibition has never been investigated in human myocardium.
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