Loss of Elmsan1 in cardiomyocytes leads to age-dependent cardiac dysfunction and reduced lifespan.

Meimei Wang, Hui Li, Chaoshan Han, Yunxi Chen, Lihao He, Min Xie, Hind Lal, Vladimir G Fast, Douglas R Moellering, Jianyi Zhang, Rui Lu, Martin Young, Yang Zhou

Department of Biomedical Engineering, Heersink School of Medicine, School of Engineering, University of Alabama at Birmingham, Birmingham, Alabama, United States.Department of Biomedical Engineering, Heersink School of Medicine, School of Engineering, University of Alabama at Birmingham, Birmingham, Alabama, United States. · pubmed

Paper

Abstract

Histone deacetylase (HDAC) complexes regulate pathological gene programs during heart disease progression. The recently identified mitotic deacetylase complex (MiDAC), which includes DNTTIP1, ELMSAN1, and HDAC1/2, remains the least characterized among these complexes. ELMSAN1 has been implicated in left ventricular remodeling, and its global deletion in mice leads to heart malformation. To investigate its role in mouse heart, we generated cardiomyocyte-specific

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Research summary

Loss of ELMSAN1 in cardiomyocytes leads to age-dependent cardiac dysfunction and reduced lifespan. The study investigates a specific genetic factor that contributes to cardiac aging and dysfunction, which is directly related to the mechanisms of aging and lifespan extension.

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