Figure 8.

Schematic Diagram of Molecular Mechanisms Underlying Plscr4-miR-214-Regulated Cardiac Hypertrophy

Under normal conditions, Plscr4 inhibits the expression of miR-214, which is the suppresser of Mfn2, to keep mitochondrial homeostasis. When CMs are exposed to pathological stimuli, the adaptive response leads to the upregulation of Plscr4, which exerts an anti-hypertrophy effect. Meanwhile, the pro-hypertrophy signal miR-214 is also upregulated. However, with prolonged stimulus, when the upregulation of miR-214 is beyond a certain threshold, it is sufficient to counteract the function of Plscr4 activation, leading to a significant decline of Mfn2 with the unbalanced mitochondrial fusion and fission, which promotes the development of cardiac hypertrophy.