Valvular heart disease has become an important public health concern. The increased wall stress and underlying disease entity associated with mitral valve disease provide unfavorable circumstances for atrial cardiomyocytes. The expression of the
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-smooth muscle actin isoform is considered characteristic of cardiomyocyte dedifferentiation (embryonic cardiomyocyte), and cardiomyocyte dedifferentiation may indicate an adaptive state, enabling cardiomyocytes to survive despite unfavorable circumstances.