Mechanistic insights into heart failure induction in ovariectomized rats: The role of mitochondrial dysfunction

Premature menopause is recognized as a factor that increase the risk of heart failure (HF). However, the fundamental pathophysiology concerning cardiac dysfunction remains inadequately understood.

This study investigated whether cardiac function was altered in ovariectomy (OV) rats compared to controls. Female rats (n = 12) were randomly assigned into 2 groups: control (sham operation) and bilateral OV group.

The echocardiographic analysis revealed that the E and E/A were significantly decreased, while the deceleration time was significantly increased in the OV group compared to the control group, indicating the presence of HF in the OV rats. ATP levels in the myocardium were significantly decreased, and oxidative DNA damage was elevated in the OV group compared to the control group. Furthermore, the mRNA levels of peroxisome-proliferator-activated receptor-gamma (PPARγ) co-activator-1 alpha (PGC-1α) and CR6 interacting factor 1 (Crif1) were reduced in the OV group.

These findings suggest that OV may induce HF through mechanisms linked to mitochondrial dysfunction.