Molecular mechanisms and therapies of immune checkpoint inhibitor associated myocarditis: Update on recent developments

Immune checkpoint inhibitors (ICIs) enhance systemic antitumor immune responses by improving the ability of immune cells to recognize and kill tumor cells specifically. Activated T lymphocytes may target tissues and organs outside the tumor, leading to different degrees of immune-related adverse events (irAEs). Immune checkpoint inhibitor-associated myocarditis (ICIAM) is a rare irAE, with an incidence of approximately 0.04–1.7 %. However, it is the most fatal irAE and often becomes a critical cause of short-term mortality in patients. Currently, the molecular mechanisms of ICIAM involve immune damage mediated by T-cell and macrophage infiltration, the common antigen theory, and pro-inflammatory responses driven by inflammatory factors and signaling pathways. However, the specific mechanisms remain unclear. A comprehensive understanding of the pathophysiological mechanisms of ICIAM can aid in identifying biomarkers and treatment targets for irAEs, ultimately improving the survival status of patients with cancer.