Key result
Canagliflozin treatment markedly alleviated cardiac inflammation, improved cardiac function, and reduced apoptosis in mice with experimental autoimmune myocarditis.
Why the study?
Canagliflozin exerts anti-inflammatory and cardioprotective effects in heart failure, but its role in myocarditis has not been elucidated.
Does canagliflozin improve cardiac inflammation and function in experimental autoimmune myocarditis mice?
Does canagliflozin improve cardiac inflammation and function in experimental autoimmune myocarditis mice?
Canagliflozin ameliorates cardiac inflammation and apoptosis in a mouse model of experimental autoimmune myocarditis, suggesting a potential novel therapeutic application.
Hypothesis-generating for SGLT2i in autoimmune myocarditis; leaves open any clinical translation from this animal model.
Myocarditis is an inflammatory cardiovascular disease which contributes to dilated cardiomyopathy (DCM) and heart failure. Canagliflozin (CANA) exerts anti-inflammatory and cardioprotective effects in heart failure besides its hypoglycemic effect. However, the role of CANA in myocarditis has not been elucidated. In this work, CANA treatment markedly alleviated cardiac inflammation and improved cardiac function in experimental autoimmune myocarditis (EAM) mice induced by α-myosin-heavy chain peptides. The expressions of NLRP3 inflammasome complexes (NLRP3, ASC, and Caspase-1) and their downstream molecules (IL-1β, IL-18) were significantly downregulated by CANA, accompanied with reduced Th17 cell infiltration in hearts. Furthermore, Bax/Bcl-2 ratio, Cleaved Caspase-3 protein level and the percentage of TUNEL-positive myocardial cells, which usually indicated apoptosis, were reduced by CANA treatment. These findings suggest CANA could be a valuable medication for myocarditis treatment.
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Long et al. (2022) studied Experimental autoimmune myocarditis. Canagliflozin was evaluated on Cardiac inflammation and cardiac function. Canagliflozin treatment markedly alleviated cardiac inflammation, improved cardiac function, and reduced apoptosis in mice with experimental autoimmune myocarditis.
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