Figure 5.

Schematic of proposed signalling involved in ALP attenuates DCM and cardiac dysfunction via activating Nrf2 pathway. Hyperglycaemia‐induced oxidative stress destructs Nrf2 signalling by inhibiting its nuclear translocation, which concomitantly with activated autophagy and subsequently reduced HO‐1 and p62 expression, resulting in cardiomyocytes apoptosis and cardiac hypertrophy. ALP activates Nrf2 by increasing its nuclear translocation following with target on ARE elements (including p62 and HO‐1) and concomitantly normalizes autophagy, which in turns reduces myocardial oxidative stress, attenuates cardiac hypertrophy and apoptosis and eventually improves cardiac function