ArticleJournal of the American Heart Association2026
Carnosinylation of Cardiac Antigens Attenuates Immunogenic Responses and Improves Function in Failing Hearts.
Article in Journal of the American Heart Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundHeart failure is associated with the accumulation of reactive lipid peroxidation-derived aldehydes, such as acrolein, which form immunogenic protein adducts in the heart. Histidyl dipeptides, including carnosine (β-alanine-histidine), can covalently sequester these aldehydes. We tested whether increasing myocardial carnosine through β-alanine supplementation reduces aldehyde stress, limits the immunogenicity of aldehyde-modified proteins, and improves cardiac function during pressure overload-induced heart failure.
methodsMale, wild-type C57BL/6J mice underwent sham or transverse aortic constriction (TAC) surgery. β-alanine was administered in drinking water either before TAC or beginning 4 weeks after TAC and continued for the remainder of the study. Cardiac function was evaluated by echocardiography. Myocardial histidyl dipeptides and aldehyde-dipeptide conjugates were quantified by liquid chromatography with tandem mass spectrometry, and immune cell populations and CD4
resultsMyocardial carnosine and anserine levels were decreased at 3 and 8 weeks after TAC. β-alanine administered either before or after TAC increased myocardial histidyl dipeptide levels, attenuated pathological cardiac remodeling and fibrosis, and reduced protein carbonylation in failing hearts. Carnosine binding to aldehyde-modified proteins decreased their antigenic potential. In vitro, this reduced dendritic cell activation and CD4
conclusionsIncreasing myocardial carnosine mitigates aldehyde stress, reduces the immunogenicity of aldehyde modified proteins and limits maladaptive immune responses, thereby preserving cardiac function during pressure overload. These findings support β-alanine supplementation as a potential therapeutic strategy to attenuate inflammation and improve outcomes in heart failure.
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