Premium
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 , oxidative stress , programmed cell death , apoptosis , pharmacology , doxorubicin , gene silencing , biology , gene knockdown , viability assay , mitochondrial ros , cancer research , microbiology and biotechnology , mitochondrion , chemistry , medicine , endocrinology , biochemistry , mitochondrial fusion , chemotherapy , gene , mitochondrial dna , enzyme
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.