scholarly journals POLYMORPHIC VARIANTS OF G/C+915 TRANSFORMING GROWTH FACTOR BETA 1 AND ATRIAL FIBRILLATION IN PATIENTS WITH METABOLIC SYNDROME

2018 ◽  
Vol 24 (1) ◽  
pp. 93-100 ◽  
Author(s):  
Yi Ma ◽  
V. A. Ionin ◽  
E. L. Zaslavskaya ◽  
A. S. Ulitina ◽  
A. Panteleeva ◽  
...  
2010 ◽  
Vol 100 (4) ◽  
pp. 335-342 ◽  
Author(s):  
Michael Behnes ◽  
Ursula Hoffmann ◽  
Siegfried Lang ◽  
Christel Weiss ◽  
Parviz Ahmad-Nejad ◽  
...  

EP Europace ◽  
2021 ◽  
Vol 23 (Supplement_3) ◽  
Author(s):  
S Koval ◽  
LA Reznik ◽  
TG Starchenko ◽  
OV Mysnychenko ◽  
M YU Penkova

Abstract Funding Acknowledgements Type of funding sources: None. Background. Patients with essential hypertension (H), primarily men, are characterized by early formation of left ventricular hypertrophy (LVH) followed by left atrial (LA) enlargement, which significantly increases the risk of development non-valvular atrial fibrillation (nAF). The most important pathogenic factor in the development of nAF is fibrosis of the LA myocardium. One of the key profibrogenic factors is transforming growth factor beta 1(TGF-beta1). Purpose. To evaluate the blood levels of TGF-beta1 in hypertensive men with paroxysmal nAF and without AF. Methods.The study included 57 men with H grade 2–3 and with LVH (age 48 ± 4 years), of those 26 with paroxysmal nAF and 31 without AF. Controls were 26 practically healthy men. All patients with paroxysmal nAF had an at least one episode of paroxysmal AF attack with spontaneous return to normal sinus rhythm and were in sinus rhythm at the time of the assessment. Patients with valvular heart disease, heart failure, ischemic heart disease, cardiomyopathy, cardiac surgery, thyroid disease, diabetes mellitus, obesity, anemia, infectious or pulmonary diseases were not included. The examination of patients include standard methods as well as echocardiography. Levels of TGF-beta1 in blood serum were measured by immune enzyme assay. All patients included in the study received standard antihypertensive therapy. Results. It was found that the blood levels of TGF-beta1 in whole group of men with H were significantly higher (13,2 [5,3;22,5] ng/mL, р=0,034 ) than in practically healthy men (7,3 [2,3;16,5] ng/mL ). The highest blood levels of TGF-beta1 were found in hypertensive men with paroxysmal nAF (18,4 [9,2;31,8] ng/mL ) and significantly exceeded (р=0,018) those in hypertensive men without AF ( 11,6 [ 4,5;19,7] ng/mL ). The following positive correlations were found in whole group of men with H between TGF-beta1 blood levels and a number of echocardiographic parameters: LA size (LA volume/height2 ) (r = 0,510, р=0,012), LV mass index ( LV mass/BSA (g/m2) ( r = 0,411, р=0,027) and E/e′ (averaged) ratio (r = 0,357, р=0,036). Conclusion. The data obtained indicate that TGF-beta1 can play an important role, both in the pathogenesis of pathological remodeling of the LV and LA in men with H, and in the development of AF in these patients.


2021 ◽  
pp. 1-11
Author(s):  
Yingbiao Wu ◽  
Jin Can ◽  
Shuwen Hao ◽  
Xun Qiang ◽  
Zhongping Ning

<b><i>Objectives:</i></b> Angiotensin II (Ang II)-induced atrial fibrosis plays a vital role in the development of atrial fibrillation (AF). Lysyl oxidase-like 2 (LOXL2) plays an essential role in matrix remodeling and fibrogenesis, indicating it may involve fibrosis-associated diseases. This study aims to elucidate the role of LOXL2 in AF, and its specific inhibitor can suppress Ang II-induced inflammatory atrial fibrosis and attenuate the enhanced vulnerability to AF. <b><i>Methods:</i></b> Male mice C57BL/6 were subcutaneously infused with either saline or Ang II (2 mg/kg/day) for 4 weeks. DMSO or LOXL2 inhibitor LOXL2-IN-1 hydrochloride (LOXL2-IN-1) at a dose of 100 μg/kg/day were intraperitoneally injected once daily for 4 weeks. Morphological, histological, and biochemical analyses were performed. AF was induced by transesophageal burst pacing in vivo. <b><i>Results:</i></b> Expression of LOXL2 was increased in serum of AF patients and Ang II-treated mice. LOXL2-IN-1 significantly attenuated Ang II-induced AF vulnerability, cardiac hypertrophy, atrial inflammation, and fibrosis. LOXL2-IN-1 suppressed Ang II-induced expression of transforming growth factor beta-1 (TGF-β1) and collagen I and phosphorylation of Smad2/3 in atrial tissue. <b><i>Conclusions:</i></b> LOXL2 is a target of AF, and its inhibitor prevents atrial fibrosis and attenuated enhanced vulnerability to AF potentially through the TGF-β/Smad pathway.


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