Hyperbaric Oxygen Therapy in Experimental Autoimmune Myocarditis: Insights from Preclinical Models to Translational Perspectives

Myocarditis is still a major global health issue that frequently manifests due to oxidative stress, immune-mediated myocardial damage, and unpredictable clinical progression. Experiments with autoimmune myocarditis (EAM) models have shown different ways that T-cell subsets, proinflammatory cytokines, macrophage polarization, and mitochondrial dysfunction are all connected and play a part in both acute inflammation and chronic remodeling of the heart. As a possible multimodal intervention that could affect several of these disease-causing pathways, hyperbaric oxygen therapy (HBOT) has become popular. This therapy delivers 100% oxygen to different tissues at higher atmospheric pressures. Early research shows that HBOT improves the delivery of oxygen to the inflamed myocardium, suppress the activation of NF-κB and NLRP3 inflammasomes, lowers oxidative stress, protects mitochondrial function, and boosts immune-regulatory T-cell responses. Despite these potentially promising findings, there are still a number of important translational obstacles to overcome, such as inconsistent protocols, a lack of long-term outcome data, insufficient mechanistic profiling, and doubts about the best protocol length and patient selection. To assess safety and effectiveness in human myocarditis, future studies should aim to integrate multi-omics analyses, HBOT regimens that are already standardized, sophisticated imaging, and carefully planned early-phase clinical trials. Overall, the currently available evidence supports HBOT as a biologically plausible and potentially valuable adjunct therapy for autoimmune myocarditis, expressing the need for further mechanistic and clinical investigation.