Figure 7.

Illustration of the role of iPLA₂β on ER stress in cardiomyocyte upon I//R. PLA₂ expression is up-regulated in cardiomyocyte after I/R, which consequently leads to an increase of phosphatidylcholine (PC) metabolism. The generation of LPC is elevated and cardiomyocyte damage is augmented. The protein level of intracellular iPLA₂β, one of the PLA₂ enzymes, is upregulated. The increased iPLA₂β translocates to the ER and induces ER stress, which further leads to apoptosis through the PERK/ATF4/CHOP pathway. Additionally, iPLA₂β may also increase intracellular calcium flow in cardiomyocyte.