Signalling mechanisms underlying doxorubicin and Nox2 NADPH oxidase‐induced cardiomyopathy: involvement of mitofusin‐2 | Zendy

McLaughlin Declan | Zendy; Zhao Youyou | Zendy; O'Neill Karla M | Zendy; Edgar Kevin S | Zendy; Dunne Philip D | Zendy; Kearney Anna M | Zendy; Grieve David J | Zendy; McDermott Barbara J | Zendy

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Signalling mechanisms underlying doxorubicin and Nox2 NADPH oxidase‐induced cardiomyopathy: involvement of mitofusin‐2

Author(s) -

McLaughlin Declan,

Zhao Youyou,

O'Neill Karla M,

Edgar Kevin S,

Dunne Philip D,

Kearney Anna M,

Grieve David J,

McDermott Barbara J

Publication year - 2017

Publication title -

british journal of pharmacology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.432

H-Index - 211

eISSN - 1476-5381

pISSN - 0007-1188

DOI - 10.1111/bph.13773

Subject(s) - nadph oxidase , mfn2 , superoxide , doxorubicin , pharmacology , oxidative stress , programmed cell death , apoptosis , gene knockdown , gene silencing , mitochondrial ros , viability assay , biology , cancer research , mitochondrion , microbiology and biotechnology , chemistry , medicine , endocrinology , biochemistry , mitochondrial fusion , chemotherapy , gene , enzyme , mitochondrial dna

The anthracycline doxorubicin (DOX), although successful as a first-line cancer treatment, induces cardiotoxicity linked with increased production of myocardial ROS, with Nox2 NADPH oxidase-derived superoxide reported to play a key role. The aim of this study was to identify novel mechanisms underlying development of cardiac remodelling/dysfunction further to DOX-stimulated Nox2 activation.

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