emerin and Atrial-Remodeling

Alteration of the nuclear Ca

Topics: Active Transport, Cell Nucleus; Angiotensin II; Aniline Compounds; Animals; Atrial Remodeling; Calcium; Cardiomegaly; Cytoplasm; Disease Models, Animal; Endothelin-1; Fluorescent Dyes; Gene Expression Regulation; Heterocyclic Compounds, 3-Ring; Humans; Membrane Proteins; Muscular Dystrophy, Emery-Dreifuss; Myocardium; Myocytes, Cardiac; Nuclear Envelope; Nuclear Proteins; Phenylephrine; Primary Cell Culture; Rats; Rats, Sprague-Dawley; RNA, Small Interfering; Ventricular Remodeling; Xanthenes

We reviewed recent advancements in the relationship between sinus node dysfunction (SND) and atrial fibrillation (AF) and propose some underlying mechanisms in regard to ion and molecular aspects. The amount of clinical and animal experiments have proven the structural and electrophysiological remodeling of sinoatrial node (SAN) and atrium may be related significantly between SND and AF. Atrial remodeling was often related to RAS activation. RAS inhibitors and statin, which resist in atrial fibrosis, may be novel strategies to prevent or treat both SND and AF. Besides, funny current (If) and Ca(2+) clock mainly contributing to the SAN automaticity may be another link between SND and AF. Gap junctions such as Cx40, Cx43 and Cx45 were proven to participate in both automaticity and conductivity of electrical impulses in SAN and atrial tissue, which was accepted as another link between SND and AF. Common genetic mutations such as the emerin gene, SCN5A gene and HCN4 gene mutation were also the mechanism for the correlation between SND and AF.

Topics: Animals; Atrial Fibrillation; Atrial Remodeling; Gap Junctions; Heart Conduction System; Humans; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels; Membrane Proteins; Models, Cardiovascular; Muscle Proteins; NAV1.5 Voltage-Gated Sodium Channel; Nuclear Proteins; Potassium Channels; Sick Sinus Syndrome; Sinoatrial Node