FIGURE 5.

Schematic representation of JNK interaction with autophagic flux and its biological functions in Nobiletin‐modulated AMI protection. The activated JNK by ROS accumulation could mediate the blockage of autophagic flux, which could exacerbate the production of ROS, leading to a feedforward loop of JNK activation. Nobiletin treatment could alleviate the activation of JNK, which help to curb the ensuing autophagic cell death and caspase‐dependent apoptosis. A recent study also suggest a possible role of increasing cardiomyocyte contractility by JNK inhibition ⁵⁴