Xiangheng Cai

1 Introduction Ischemic heart disease, particularly acute myocardial infarction (AMI), remains one of the leading causes of death worldwide [1-3]. While reperfusion therapies have significantly reduced early mortality rates, the incidence of post-MI heart failure continues to rise, underscoring the unmet need for therapies that reduce adverse ventricular remodeling [4, 5]. Following AMI, the cardiac inflammatory response initiates ventricular remodeling [6, 7].

Introduction Islet transplantation has emerged as a promising therapeutic option for type 1 diabetes (T1D), offering the potential for insulin independence and improved glycemic control (1, 2). Despite these promising outcomes, the success of intrahepatic islet transplantation is often compromised by a complex and detrimental immune response known as the instant blood-mediated inflammatory reaction (IBMIR), a severe immune response that occurs immediately post-transplantation (3).