Myocardial G protein-coupled receptor kinase 5 contributes to impaired cardiac function and immune cell recruitment in ischemic heart failure. Myocardial G protein-coupled receptor kinase 5 contributes to impaired cardiac function and immune cell recruitment in ischemic heart failure

Myocardial ischemia (MI) is the most common cause of heart failure (HF) in the United States. G protein‑coupled receptor (GPCR) kinase 5 (GRK5) has been found to be upregulated in failing human myocardium. While the canonical role of GRKs is to desensitize receptors via phosphorylation, GRK5 can also translocate to the nucleus of cardiomyocytes where it exerts GPCR‑independent effects that promote maladaptive cardiac hypertrophy. The role of GRK5 in ischemic heart disease is still unknown Overall design: RNA-seq on cardiomyocytes from control (NLC) and Grk5-transgenic (TgGRK5) mice 4 days after myocardial infraction (MI)