Immune checkpoint inhibitors (ICIs) have transformed cancer therapy but can induce immune-related myocarditis (ICI-MC), a rare yet life-threatening toxicity. This review elucidates the cellular and molecular mechanisms underlying ICI-MC, integrating insights from T-cell dysregulation, innate immunity, and stromal interactions. Pathogenesis involves α-myosin-driven clonal expansion of cytotoxic CD8+ T cells, loss of regulatory subsets, and macrophage polarization toward M1 phenotypes via cGAS-STING and STAT1/NF-κB pathways. Crosstalk among macrophages, fibroblasts, endothelial cells, neutrophils, and B cells amplifies myocardial inflammation through chemokine and complement activation. A five-phase multicellular framework-baseline autoreactivity, checkpoint blockade, clonal expansion, effector execution, and inflammatory amplification-summarizes disease evolution. Candidate biomarkers and targeted therapies offer precision strategies to mitigate cardiotoxicity. Future single-cell and multi-omics studies are essential to refine diagnosis and develop cardioprotective interventions without compromising antitumor efficacy.