IL6 and myocardial infarction: Blockade of A2bAR inhibited caspase-1 activity and leukocyte infiltration and attenuated the secretion of pro-fibrotic and pro-inflammatory mediators, such as transforming growth factor-beta, interleukin 6 (IL-6), and tumor necrosis factor-alpha, after myocardial infarction via the PKC-delta pathway (Alter et al., 2023; Feng et al., 2010).