title: TGF-β1 signal pathway in the regulation of inflammation in patients with atrial fibrillation.
abstract: OBJECTIVE
  To observe the expression changes of inflammatory markers TGF-β1, Smad3 and IL-6 in patients with atrial fibrillation (AF), and to explore the significance of TGF-β1 signaling pathway in the structural remodeling of AF.
  
  
  METHODS
  The expression of TGF-β1, Smad3 and IL-6 in 50 cases with AF and 30 normal cases were detected by RT-PCR and ELISA.
  
  
  RESULTS
  The TGF-β1, Smad3 and IL-6 mRNA and protein expression levels in patients with AF were significantly higher than that in the control group (P<0.05), but there was no significantly different between the paroxysmal AF group and the persistent AF group (P>0.05). The TGF-β1mRNA expression in the ⩾ 50 years subgroup was significantly higher than that in the <50 years subgroups, and it was higher in the NYHA III subgroup than in the I/II grade subgroup. It was also higher in the left ventricular ejection fraction (LVEF) <50% subgroup than in LVEF ⩾ 50% group, and it was significantly higher in the AF time ⩾ 36 months subgroup than that in <36 months subgroup (P<0.05). The Smad3 and IL-6 expressions in the in the LVEF <50% subgroup were both high that than that in LVEF ⩾ 50% group, and higher in the AF time ⩾ 36 months subgroup than that in <36 months subgroup (P<0.05). There were a positive correlation between TGF-β1, Smad3 and IL-6 (r=0.687, r=0.547). There were also a positive correlation between Smad3 and IL-6 mRNA (r=0.823).
  
  
  CONCLUSIONS
  AF is associated with inflammation, and the inflammation is also involved in the fibrillation and sustain of AF. The TGF-β1 signal pathway may be involved in the process of atrial structural remodeling in patients with AF, and iss related with the occurrence and maintenance of AF.
authors.affiliation: Comprehensive Cardiology Department, First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830011, China.
authors.forename: Ye Erbo Lati Ali
authors.initials: YE
authors.lastname: Mira
authors.lastname: Muhuyati
authors.forename: Wu-Hong
authors.initials: WH
authors.lastname: Lu
authors.forename: Peng-Yi
authors.initials: PY
authors.lastname: He
authors.forename: Zhi-Qiang
authors.initials: ZQ
authors.lastname: Liu
authors.forename: Yu-Chun
authors.initials: YC
authors.lastname: Yang
mesh_terms: D000328:Adult; D000368:Aged; D001281:Atrial Fibrillation / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D005260:Female; D006439:Hemodynamics; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000378:metabolism*; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D015398:Signal Transduction / Q000502:physiology*; D051900:Smad3 Protein / Q000097:blood / Q000235:genetics / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000097:blood* / Q000235:genetics / Q000378:metabolism
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; C497790:SMAD3 protein, human; D051900:Smad3 Protein; D053773:Transforming Growth Factor beta1
keywords: Atrial fibrillation; Inflammation; Signal transduction; Transforming growth factor β1