S100A8 and myocardial infarction: Du et al. found that S100A8/A9 was continuously expressed in mouse hearts during the early stages of myocardial ischemia/reperfusion injury (MI/RI) by time-series transcriptomics analysis, peaked at 6 h after reperfusion, and returned to baseline levels on day 7, thus clarifying that S100A8/A9 is an early mediator of I/R injury and is rapidly elevated in the early stages of MI/RI (65).