Myocarditis remains a significant global health burden often accompanied by im-mune-mediated myocardial injury, oxidative stress, and unpredictable clinical progres-sion. Experimental autoimmune myocarditis (EAM) models have provided different in-sights into the interconnected roles of T-cell subsets, proinflammatory cytokines, mac-rophage polarization, and mitochondrial dysfunction in both acute inflammation and chronic cardiac remodeling. Hyperbaric oxygen therapy (HBOT), which delivers 100% oxygen at elevated atmospheric pressures, has emerged as a potential multimodal in-tervention capable of affecting several of these pathogenic pathways. Preclinical data demonstrate that HBOT enhances oxygen delivery to the inflamed myocardium, sup-presses the activation of NF-κB and NLRP3 inflammasomes, reduces oxidative stress, preserves mitochondrial function, and promotes immunoregulatory T-cell responses. Despite these promising results, significant translational challenges remain, including protocol variability, lack of long-term outcome data, incomplete mechanistic profiling, and uncertainties regarding optimal timing and patient selection. Future research should try to incorporate already standardized HBOT regimens, multi-omics analyses, advanced imaging, and well-designed early-phase clinical trials to evaluate safety and efficacy in human myocarditis. Overall, the currently available evidence supports HBOT as a bi-ologically plausible and potentially valuable adjunct therapy for autoimmune myocar-ditis, expressing the need for further mechanistic and clinical investigation.