Cardiomyocytes were pretreated with 2 µM CC and stimulated with 100 nM testosterone by 24 h. A Cardiomyocytes were transfected with siRNA-control or siRNA-AMPKα2 (20 nM) and protein levels were determined by Western blot. Cardiomyocytes were transfected with siRNA-control or siRNA-AMPKα2 (20 nM) and protein levels were determined by Western blot. It has been shown that AMPK inhibition promotes ovarian angiogenesis via the AMPK–HIF-1α/vascular endothelial growth factor A/vascular endothelial growth factor receptor 2/connective tissue growth factor (AMPK-Hif-1α/Vegfa/Vegfr2/Ctgf) signalling pathway 30,33. The differential effects of AMPK on angiogenesis are mediated by cell-specific responses, environmental factors, and the balance between pro- and anti-angiogenic signalling downstream of AMPK . AMPK inhibition increases ovulation and oocyte fertilisation during in situ intrabursal injection with gonadotropin stimulation in mouse ovaries. Studies have shown that AMPK activity influences follicular development, including granulosa cell proliferation and oocyte meiotic progression. Triggered by the preovulatory gonadotrophin surge in each reproductive cycle, the dominant Graafian follicle releases a mature oocyte for potential fertilisation.
