Table 2.

Summary of the involvement of the CaM cascade in cardiovascular disease.

Kinase	In Heart Pathology	In Vasculature Pathology
CaM	Polymorphisms linked to calmodulinopathy, arrhythmia [44,45,59,60,61,62,63,64,65,66,67,68,69].	Unknown
CaMKII	Implicated in myocardial injury [116], atrial fibrillation [117], cardiac hypertrophy, ischaemia/reperfusion injury [118], heart failures, contributing to apoptosis, arrhythmias [113], defective ECC and ETC [53,114,115], pathological hypertrophy [96] and contractile dysfunction during heart failure [54,96,114,115].	Regulation of VSMCs phenotype switching through the inhibition of CREB [34].
CaMKK1	Polymorphism linked to the higher risk to develop CVD [136].	Regulation of VSMCs phenotype switching (CaMKK-CaMKIV-CREB) [34].
CaMKK2	Inactivation of CaMKK2 indirectly results in the development of metabolic dysfunction and cardiac hypertrophy [143].	Regulation of VSMCs phenotype switching (CaMKK-CaMKIV-CREB) [34].
CAMKI	Unknown	Unknown
CAMKIV	Polymorphisms linked to elevated diastolic blood pressure [162,163,164].	Regulation of VSMCs phenotype switching (CaMKK-CaMKIV-CREB) [34].