European journal of clinical investigation · 2010
Autophagy as a mechanism for myolysis of cardiomyocytes in mitral regurgitation.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Chen Mien-Cheng, Chang Jen-Ping, Wang Ya-Hui, Liu Wen-Hao, Ho Wan-Chun, Chang Hsueh-Wen
Аннотация
BACKGROUND: Myolysis of atrial cardiomyocytes occurs in patients with severe mitral and tricuspid regurgitation. This morphological remodelling may involve autophagy.
METHODS: This study comprised 20 patients (10 with long-standing persistent atrial fibrillation and 10 with sinus rhythm) with severe mitral and tricuspid regurgitation. Atrial appendageal tissues were obtained during surgery. The appearance of autophagosomes (LC3B) in myocytes can reflect autophagy induction. Complement 9 is used as a reliable marker of oncosis.
RESULTS: In the fibrillating right atria, 68·4 ± 18·9% of total myocytes showed moderate-to-severe myolysis, while 64·2 ± 15·8% of total myocytes comprised these cells in right atrial myocardium with sinus rhythm. Immunohistochemical study revealed LC3B-positive myocytes in 8·0% of myocytes without myolysis, 11·9% of myocytes with mild myolysis and 49·4% of myocytes with moderate-to-severe myolysis in right atrial myocardium with sinus rhythm (P < 0·0001). Similarly, in the fibrillating right atria, LC3B-positive myocytes were observed in 5·9% of myocytes without myolysis, 12·2% of myocytes with mild myolysis and 50·7% of myocytes with moderate-to-severe myolysis (P < 0·0001). Moreover, in the fibrillating left atria, LC3B-positive myocytes were observed in 4·9% of myocytes without myolysis, 12·6% of myocytes with mild myolysis and 52·0% of myocytes with moderate-to-severe myolysis (P < 0·0001). None of the atrial myocytes displayed intracellular deposition of complement 9.
CONCLUSIONS: Induction of autophagy, but not oncosis, occurs in most cases of atrial cardiomyocytes with severe mitral and tricuspid regurgitation, even those without atrial fibrillation, and is closely associated with the development of myolysis in this disease.
METHODS: This study comprised 20 patients (10 with long-standing persistent atrial fibrillation and 10 with sinus rhythm) with severe mitral and tricuspid regurgitation. Atrial appendageal tissues were obtained during surgery. The appearance of autophagosomes (LC3B) in myocytes can reflect autophagy induction. Complement 9 is used as a reliable marker of oncosis.
RESULTS: In the fibrillating right atria, 68·4 ± 18·9% of total myocytes showed moderate-to-severe myolysis, while 64·2 ± 15·8% of total myocytes comprised these cells in right atrial myocardium with sinus rhythm. Immunohistochemical study revealed LC3B-positive myocytes in 8·0% of myocytes without myolysis, 11·9% of myocytes with mild myolysis and 49·4% of myocytes with moderate-to-severe myolysis in right atrial myocardium with sinus rhythm (P < 0·0001). Similarly, in the fibrillating right atria, LC3B-positive myocytes were observed in 5·9% of myocytes without myolysis, 12·2% of myocytes with mild myolysis and 50·7% of myocytes with moderate-to-severe myolysis (P < 0·0001). Moreover, in the fibrillating left atria, LC3B-positive myocytes were observed in 4·9% of myocytes without myolysis, 12·6% of myocytes with mild myolysis and 52·0% of myocytes with moderate-to-severe myolysis (P < 0·0001). None of the atrial myocytes displayed intracellular deposition of complement 9.
CONCLUSIONS: Induction of autophagy, but not oncosis, occurs in most cases of atrial cardiomyocytes with severe mitral and tricuspid regurgitation, even those without atrial fibrillation, and is closely associated with the development of myolysis in this disease.