The histone 3 lysine 9 methyltransferase inhibitor chaetocin improves prognosis in a rat model of high salt diet-induced heart failure View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-12

AUTHORS

Tomohiko Ono, Naomi Kamimura, Tomohiro Matsuhashi, Toshihiro Nagai, Takahiko Nishiyama, Jin Endo, Takako Hishiki, Tsuyoshi Nakanishi, Noriaki Shimizu, Hirotoshi Tanaka, Shigeo Ohta, Makoto Suematsu, Masaki Ieda, Motoaki Sano, Keiichi Fukuda, Ruri Kaneda

ABSTRACT

Histone acetylation has been linked to cardiac hypertrophy and heart failure. However, the pathological implications of changes in histone methylation and the effects of interventions with histone methyltransferase inhibitors for heart failure have not been fully clarified. Here, we focused on H3K9me3 status in the heart and investigated the effects of the histone H3K9 methyltransferase inhibitor chaetocin on prognoses in Dahl salt-sensitive rats, an animal model of chronic heart failure. Chaetocin prolonged survival and restored mitochondrial dysfunction. ChIP-seq analysis demonstrated that chronic stress to the heart induced H3K9me3 elevation in thousands of repetitive elements, including intronic regions of mitochondria-related genes, such as the gene encoding peroxisome proliferator-activated receptor-gamma coactivator 1 alpha. Furthermore, chaetocin reversed this effect on these repetitive loci. These data suggested that excessive heterochromatinization of repetitive elements of mitochondrial genes in the failing heart may lead to the silencing of genes and impair heart function. Thus, chaetocin may be a potential therapeutic agent for chronic heart failure. More... »

PAGES

39752

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/srep39752

DOI

http://dx.doi.org/10.1038/srep39752

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1036676827

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28051130


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