New mechanisms: From lactate to lactylation to rescue heart failure

Linfeng Yi; Dan Tang; Xing Xiang; Chungang Xiao; Huifang Tang; Hong Huang

doi:10.5582/bst.2024.01000

This article has now been updated. Please use the final version.

New mechanisms: From lactate to lactylation to rescue heart failure

Linfeng Yi, Dan Tang, Xing Xiang, Chungang Xiao, Huifang Tang, Hong Huang

Author information

Linfeng Yi
Department of Clinical Laboratory Medicine, Institution of microbiology and infectious diseases, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Clinical Research Center for Myocardial Injury in Hunan Province, Hengyang, Hunan, China.
Institute of Cardiovascular Disease, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Hunan Provincial Key Laboratory of Multi-omics And Artificial Intelligence of Cardiovascular Diseases, University of South China, Hengyang, Hunan, China.
Dan Tang
Department of Clinical Laboratory Medicine, Institution of microbiology and infectious diseases, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Clinical Research Center for Myocardial Injury in Hunan Province, Hengyang, Hunan, China.
Institute of Cardiovascular Disease, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Hunan Provincial Key Laboratory of Multi-omics And Artificial Intelligence of Cardiovascular Diseases, University of South China, Hengyang, Hunan, China.
Xing Xiang
Department of Clinical Laboratory Medicine, Institution of microbiology and infectious diseases, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Clinical Research Center for Myocardial Injury in Hunan Province, Hengyang, Hunan, China.
Institute of Cardiovascular Disease, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Hunan Provincial Key Laboratory of Multi-omics And Artificial Intelligence of Cardiovascular Diseases, University of South China, Hengyang, Hunan, China.
Chungang Xiao
Department of Cardiology, Hunan University of Medicine General Hospital, Huaihua, Hunan, China.
Huifang Tang
Clinical Research Center for Myocardial Injury in Hunan Province, Hengyang, Hunan, China.
Institute of Cardiovascular Disease, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Hunan Provincial Key Laboratory of Multi-omics And Artificial Intelligence of Cardiovascular Diseases, University of South China, Hengyang, Hunan, China.
Department of Cardiology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Hong Huang
Clinical Research Center for Myocardial Injury in Hunan Province, Hengyang, Hunan, China.
Institute of Cardiovascular Disease, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Hunan Provincial Key Laboratory of Multi-omics And Artificial Intelligence of Cardiovascular Diseases, University of South China, Hengyang, Hunan, China.

Keywords: α-MHC, lactylation, sarcomeric structure and function, heart failure, Titin

JOURNAL FREE ACCESS Advance online publication

Article ID: 2024.01000

DOI https://doi.org/10.5582/bst.2024.01000

The final version of this article is now available: Vol. 18 (2024), No. 1 pp. 105-107

Details

Abstract

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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