ObjectiveTo investigate the regulatory mechanism of transforming growth factor-β1 (TGF-β1) in different types of mitral valvular disease (MVD) with atrial fibrillation (AF). MethodsFrom August 2011 to August 2012, 16 patients with moderate to severe MVD accompanied by AF who required mitral valve replacement at the Department of Cardiovascular Surgery, West China Hospital, Sichuan University, were included. Based on echocardiographic results, patients were divided into two groups: a mitral regurgitation (MR) with AF (MR-AF) group and a mitral stenosis (MS) with AF (MS-AF) group. Left atrial tissue samples were collected during surgery. Techniques such as enzyme-linked immunosorbent assay, real-time fluorescence quantitative polymerase chain reaction, immunohistochemistry, and Western blotting were used to detect key molecules in the TGF-β1/JNK pathway. ResultsThere were 8 patients in the MR-AF group, including 5 males and 3 females, with an average age of (41.38±11.19) years; and 8 patients in the MS-AF group, including 6 males and 2 females, with an average age of (43.12±5.30) years. The left atrial volume load was higher in MR-AF patients, while the left atrial pressure load was higher in MS-AF patients. In MS-AF patients, the relative expression levels of MAPK9, JUN, CASP3, BAX, and BCL2 mRNA in left atrial tissues were significantly upregulated. The serum TGF-β1 protein level and the relative expression levels of p-JNK, p-c-Jun, and Caspase-3 proteins in the left atrial tissues of the MR-AF group were higher. Myocardial cell damage was more severe in the MS-AF group, and the expression level of Bcl-2 was higher. ConclusionDifferent mitral valve lesions have distinct hemodynamic characteristics. The myocardium of the left atrium in MR-AF patients is more prone to apoptosis, possibly through the activation of the TGF-β1/JNK signaling pathway.
Atrial fibrillation(AF) is the most common disorder of cardiac rhythm. It has a high morbidity, mortality and disability, and serious impact on quality of life of patients. It is demonstrated that atrial remodeling which includes atrial electrical remodeling and structural remodeling,are the central contributors to the development and selfperpetuating of AF. However, The mechanisms that underlie the atrial remodeling process in AF have not yet been completely elucidated. New strategies for the prevention and termination of AF should build on our knowledge of the mechanisms of atrial remodeling. Medication for the reversal of atrial remodeling may be the new target for the treatment of AF. At present, drugs that target atrial remodeling have already obtained fruitful results in the experimental and clinical investigations. Now some recent advancements of this area is reviewed in this article.