CX3CR1 and myocardial infarction: Similarly, their protective effects have been also presented in a murine model of MI, despite the significant loss of Cx3Cr1+ cells during maturation, with limited self-renewal capacity and regenerative potential, selective depletion of this population in adult hearts leads to impaired cardiac function and remodeling following ischemic cardiac injury, indicating that Cx3Cr1+ cells still play a role in wound healing in the adult heart [38, 71, 137].