DNA single-strand break-induced DNA damage response causes heart failure View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-04-24

AUTHORS

Tomoaki Higo, Atsuhiko T. Naito, Tomokazu Sumida, Masato Shibamoto, Katsuki Okada, Seitaro Nomura, Akito Nakagawa, Toshihiro Yamaguchi, Taku Sakai, Akihito Hashimoto, Yuki Kuramoto, Masamichi Ito, Shungo Hikoso, Hiroshi Akazawa, Jong-Kook Lee, Ichiro Shiojima, Peter J. McKinnon, Yasushi Sakata, Issei Komuro

ABSTRACT

The DNA damage response (DDR) plays a pivotal role in maintaining genome integrity. DNA damage and DDR activation are observed in the failing heart, however, the type of DNA damage and its role in the pathogenesis of heart failure remain elusive. Here we show the critical role of DNA single-strand break (SSB) in the pathogenesis of pressure overload-induced heart failure. Accumulation of unrepaired SSB is observed in cardiomyocytes of the failing heart. Unrepaired SSB activates DDR and increases the expression of inflammatory cytokines through NF-κB signalling. Pressure overload-induced heart failure is more severe in the mice lacking XRCC1, an essential protein for SSB repair, which is rescued by blocking DDR activation through genetic deletion of ATM, suggesting the causative role of SSB accumulation and DDR activation in the pathogenesis of heart failure. Prevention of SSB accumulation or persistent DDR activation may become a new therapeutic strategy against heart failure. More... »

PAGES

15104

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ncomms15104

    DOI

    http://dx.doi.org/10.1038/ncomms15104

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1085049585

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/28436431


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