PMID- 17689021
OWN - NLM
STAT- MEDLINE
DCOM- 20080502
LR  - 20080903
IS  - 0306-9877 (Print)
IS  - 0306-9877 (Linking)
VI  - 70
IP  - 2
DP  - 2008
TI  - The fibrosis and atrial fibrillation: is the transforming growth factor-beta 1 a 
      candidate etiology of atrial fibrillation.
PG  - 317-9
AB  - 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.
FAU - Li, Xuping
AU  - Li X
AD  - Department of Cardiology, Beijing AnZhen Hospital, Capital Medical University, 
      Beijing 100029, PR China.
FAU - Ma, Changsheng
AU  - Ma C
FAU - Dong, Jianzeng
AU  - Dong J
FAU - Liu, Xingpeng
AU  - Liu X
FAU - Long, Deyong
AU  - Long D
FAU - Tian, Yin
AU  - Tian Y
FAU - Yu, Ronghui
AU  - Yu R
LA  - eng
PT  - Journal Article
DEP - 20070803
PL  - United States
TA  - Med Hypotheses
JT  - Medical hypotheses
JID - 7505668
RN  - 0 (Angiotensin-Converting Enzyme Inhibitors)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Transforming Growth Factor beta1)
SB  - IM
CIN - Med Hypotheses. 2008;71(1):149-50. PMID: 18329183
MH  - Angiotensin-Converting Enzyme Inhibitors/pharmacology
MH  - Animals
MH  - Antibodies, Monoclonal/pharmacology
MH  - Atrial Fibrillation/*etiology/pathology/physiopathology/therapy
MH  - Fibrosis
MH  - Humans
MH  - Models, Cardiovascular
MH  - Myocardium/pathology
MH  - Transforming Growth Factor beta1/antagonists & inhibitors/immunology/*physiology
EDAT- 2007/08/11 09:00
MHDA- 2008/05/03 09:00
CRDT- 2007/08/11 09:00
PHST- 2007/04/10 00:00 [received]
PHST- 2007/04/17 00:00 [accepted]
PHST- 2007/08/11 09:00 [pubmed]
PHST- 2008/05/03 09:00 [medline]
PHST- 2007/08/11 09:00 [entrez]
AID - S0306-9877(07)00383-0 [pii]
AID - 10.1016/j.mehy.2007.04.046 [doi]
PST - ppublish
SO  - Med Hypotheses. 2008;70(2):317-9. doi: 10.1016/j.mehy.2007.04.046. Epub 2007 Aug 
      3.