Key result
Lactylation of α-myosin heavy chain enhances its interaction with Titin to maintain sarcomeric structure, and administering lactate or inhibiting lactate efflux alleviates heart failure in mice.
Why the study?
Does the administration of lactate or inhibition of lactate efflux improve heart failure symptoms by restoring α-MHC lactylation in mice with heart failure?
Does the administration of lactate or inhibition of lactate efflux improve heart failure symptoms by restoring α-MHC lactylation in mice with heart failure?
Lactylation of α-MHC preserves sarcomeric structure and function, presenting a novel therapeutic target for heart failure through lactate administration or efflux inhibition.
Lactylation of α-myosin heavy chain (α-MHC) has recently been reported to preserve sarcomeric structure and function and attenuate the development of heart failure. Specifically, lactylation enhanced the interaction of α-MHC with the sarcomeric protein Titin, thereby maintaining normal sarcomeric structure and myocardial contractile function. Furthermore, the administration of lactate or inhibition of lactate efflux potentially treats heart failure by restoring lactylation of α-MHC and the interaction of α-MHC with Titin. This finding highlights the significant role of α-MHC lactylation in myocardial diseases and presents a new therapeutic target for the treatment of heart failure.
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Yi et al. (2024) conducted a letter in Heart failure. Sodium lactate (NALA) and VB124 was evaluated. Lactylation of α-myosin heavy chain enhances its interaction with Titin to maintain sarcomeric structure, and administering lactate or inhibiting lactate efflux alleviates heart failure in mice.
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