Ataxia telangiectasia mutated in cardiac fibroblasts regulates doxorubicin-induced cardiotoxicity | Zendy

Hong Zhan | Zendy; Kenichi Aizawa | Zendy; Junqing Sun | Zendy; Shota Tomida | Zendy; Kinya Otsu | Zendy; Simon J. Conway | Zendy; Peter J. McKin | Zendy; Ichiro Manabe | Zendy; Issei Komuro | Zendy; Kiyoshi Miyagawa | Zendy; Ryozo Nagai | Zendy; Toru Suzuki | Zendy

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Ataxia telangiectasia mutated in cardiac fibroblasts regulates doxorubicin-induced cardiotoxicity

Author(s) -

Hong Zhan,

Kenichi Aizawa,

Junqing Sun,

Shota Tomida,

Kinya Otsu,

Simon J. Conway,

Peter J. McKin,

Ichiro Manabe,

Issei Komuro,

Kiyoshi Miyagawa,

Ryozo Nagai,

Toru Suzuki

Publication year - 2016

Publication title -

cardiovascular research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.774

H-Index - 219

eISSN - 1755-3245

pISSN - 0008-6363

DOI - 10.1093/cvr/cvw032

Subject(s) - cardiotoxicity , doxorubicin , ataxia telangiectasia , apoptosis , cancer research , oxidative stress , pharmacology , medicine , fibroblast , biology , dna damage , endocrinology , chemotherapy , cell culture , biochemistry , dna , genetics

Doxorubicin (Dox) is a potent anticancer agent that is widely used in the treatment of a variety of cancers, but its usage is limited by cumulative dose-dependent cardiotoxicity mainly due to oxidative damage. Ataxia telangiectasia mutated (ATM) kinase is thought to play a role in mediating the actions of oxidative stress. Here, we show that ATM in cardiac fibroblasts is essential for Dox-induced cardiotoxicity.

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