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In a study of experimental autoimmune myocarditis induced by cardiac troponin-I immunization (CTPN: SMD: 37.93, 95% CI 4.28, 71.58, p = 0.03), both the biomolecules, HMGB1 and RAGE (not computed) were considered as potential therapeutic targets in heart failure treatment, given the ability of HMGB1 to stimulate immunity and their ability to interact with each other, RAGE being its principal binding partner in both preclinical and clinical studies

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