Myeloid Cell-Derived S100a9 Modulates The Expression Of Histone Methylation Epigenetic Enzymes In The Myocardium After Permanent Ischemia In Mice

Background and Aims: Histone methylation-related epigenetic pathways have emerged as potential drug targets in cardiovascular diseases; however their implication in the pathology of myocardial infarction (MI) is largely unknown. The neutrophil-derived alarmin S100A8/A9 initiates and amplifies the inflammatory reactions in MI. Thus, we questioned whether in MI a mechanistic link exists between S100A9 and the expression of archetypal histone methylation enzymes.