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Previous studies found that mitochondrial tRNA mutation with high salt stimulation can contribute to high blood pressure; however, the mechanism of increased hypertension-induced cardiac injury remains unclear.
Spontaneously hypertensive rats (SHR) were divided into 4 groups: SHR, SHR with high salt stimulation (SHR+NaCl), SHR carrying tRNA mutations (SHR+M) and SHR+M with high salt stimulation (SHR+M+NaCl). Healthy Wistar-Kyoto (WKY) rats served as controls.
The left ventricular mass and interventricular septum was highest in the SHR+M+NaCl group (P<0.05), while ejection fraction was lowest in the SHR+M+NaCl group (P<0.05). H&E staining showed degree of hypertrophy of myocardial cells with interstitial fibrosis and localized inflammatory cell infiltration in hypertensive groups, especially in SHR+M+NaCl group. Electron microscopy showed that mitochondria of the cardiac tissue of hypertensive groups had different degrees of cavitation most obviously affected in SHR+M+NaCl group. ROS levels in the hypertensive groups were significantly highest in the SHR+M+NaCl groups (P<0.05). The expression of voltage dependent anion channel (VDAC) and Bax associated with apoptosis were also obviously highest in the SHR+M+NaCl group (P<0.05). Colocalization of VDAC and Bax was obviously noticed in the SHR+M+NaCl groups but not the control group (P<0.05).
Therefore, mitochondrial tRNA mutation with high salt stimulation could aggravate cardiac damage, which was associated with the increased expression and interaction between Bax and VDAC, promoting the formation of ROS and potentially the initiating apoptosis.