Molecular Mechanisms of Atrial Fibrillation Essay

Molecular Mechanisms of Atrial Fibrillation - Essay Example Progression in the studies of genetics and molecular biology would assist in dealing with this disease in a better way. Recently studies by Chelu et al (2009) have brought into light the fact that differences in the ionic (mainly Ca 2+) current flow are responsible for causing AF and turning it into a chronic condition. As Brugada points out â€Å"Research efforts to elucidate the molecular basis of AF are focused into two main areas: human genetics and alterations in genetic expression of ion channels† (Brugada, Is Atrial fibrillation a genetic disease?: Molecular Mechanisms in Arial fibrillation). The beating of the heart muscles, according to research, is strictly controlled by a procedure known as ‘Ca 2+ induced Ca 2+ release’. Here we find that the number of Ca ions that are entering through the Cav. 1.2 which is the L type voltage gated Ca ion channel helps in the increase of the release of more Ca ions from the sarcoplasmic reticulum through the intracellular Ca 2+ channels (ryanodine receptor type 2 or RyR2). This influx and release of Ca ions are strictly regulated by the heart muscles for the controlled beating of heart. In AF, where the atria beats rapidly, this rapid beating of the heart leads to production of more Ca ions or Calmodulin- dependent protein kinase II ( CaMKII) phosphorylation of the RyR2. In AF conditions it has also been noticed that L type voltage gated Ca ion channels show a decrease in its amplitude, so it has been deduced that this release of the Ca ions may be due to enhanced functioning of RyR2 channels. There are many reasons as t o why the RyR2 channels may function differently. Earlier it was seen in researches conducted on dogs showing AF conditions, that RyR2 channels remained open in cases having low cystolic Ca ion presence. Another reason as Vest, et al, tells us from his experiments into molecular mechanisms that â€Å"SR Ca2+  leak due to RyR2