title: The fibrosis and atrial fibrillation: is the transforming growth factor-beta 1 a candidate etiology of atrial fibrillation.
abstract: Atrial fibrillation (AF) is the most commonly occurring arrhythmia in clinical practice, however, the mechanism of atrial fibrillation is not well explained. It has been considered that myocardial fibrosis plays a role in atrial fibrillation. Within the heart, this fibrosis is thought to be mediated by transforming growth factor-beta 1 (TGF-beta 1), a potent stimulator of collagen-producing cardiac fibroblasts. Recent studies indicate that atrial fibrillation is associated with elevated serum concentrations of TGF-beta 1 and C-terminal propeptide of procollagen type I (a marker of collagen type I synthesis). TGF-beta 1 was not only associated with the presence of atrial fibrillation but may also predict patients at increased risk for future development of atrial fibrillation. Why TGF-beta 1 in atrial fibrillation is high is a puzzling problem. We hypothesized that TGF-beta 1 is a possible cause of atrial fibrillation by initiating fibrosis response. Atrial interstitial fibrosis has been seen in patients with CHF and in animal models of pacing-induced heart failure. It was demonstrated that TGF-beta 1 levels were increased in the atria after the development of congestive heart failure in dogs. In a similar study, mice with increased expression of TGF-beta 1 were prone to atrial fibrillation development as a result of raised levels of atrial fibrosis. If the hypothesis is confirmed, administration of TGF-beta 1 monoclonal antibodies may be used to eliminate the etiology. It will be a new target point to treat atrial fibrillation.
authors: Department of Cardiology, Beijing AnZhen Hospital, Capital Medical University, Beijing 100029, PR China.
authors: Xuping
authors: X
authors: Li
authors: Changsheng
authors: C
authors: Ma
authors: Jianzeng
authors: J
authors: Dong
authors: Xingpeng
authors: X
authors: Liu
authors: Deyong
authors: D
authors: Long
authors: Yin
authors: Y
authors: Tian
authors: Ronghui
authors: R
authors: Yu
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D001281:Atrial Fibrillation / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D005355:Fibrosis; D006801:Humans; D008955:Models, Cardiovascular; D009206:Myocardium / Q000473:pathology; D053773:Transforming Growth Factor beta1 / Q000037:antagonists & inhibitors / Q000276:immunology / Q000502:physiology*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000911:Antibodies, Monoclonal; D053773:Transforming Growth Factor beta1