The fibrosis and atrial fibrillation: is the transforming growth factor-beta 1 a candidate etiology of atrial fibrillation.
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.
Li
Xuping
X
Department of Cardiology, Beijing AnZhen Hospital, Capital Medical University, Beijing 100029, PR China.
Ma
Changsheng
C
Dong
Jianzeng
J
Liu
Xingpeng
X
Long
Deyong
D
Tian
Yin
Y
Yu
Ronghui
R
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*
D000806:Angiotensin-Converting Enzyme Inhibitors; D000911:Antibodies, Monoclonal; D053773:Transforming Growth Factor beta1