Open AccessCathepsin B aggravated doxorubicin‑induced myocardial injury via NF‑κB signalling
Author(s) -
Chen Liu,
Zhulan Cai,
Te Hu,
Yanfei Qi,
Lijun Zhang
Publication year - 2020
Publication title -
molecular medicine reports
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2020.11583
Subject(s) - cathepsin b , oxidative stress , apoptosis , cardiotoxicity , doxorubicin , cancer research , small interfering rna , cathepsin d , programmed cell death , microbiology and biotechnology , biology , transfection , cell culture , endocrinology , biochemistry , genetics , chemotherapy , enzyme
Myocyte apoptosis and oxidative stress key critical roles in the process of doxorubicin (DOX)‑induced cardiotoxicity. However, how apoptosis and oxidative stress arise in DOX‑induced heart injury remains largely unknown. Cathepsin B (CTSB) is a typical lysosomal cysteine protease that is associated with apoptosis, inflammatory responses, oxidative stress and autophagy. The present study aimed to investigate the role of CTSB in DOX‑induced heart injury and its potential mechanism. H9C2 cells were infected with adenovirus or transfected with small interfering RNA to overexpress or knock down CTSB, respectively, and then stimulated with DOX. DOX induced increased CTSB expression levels in H9C2 cells. DOX‑induced cardiomyocyte apoptosis and oxidative stress were attenuated by CTSB knockdown but aggravated by CTSB overexpression in vitro. Mechanistically, the present study showed that CTSB activated the NF‑κB pathway in response to DOX. In summary, CTSB aggravated DOX‑induced H9C2 cell apoptosis and oxidative stress via NF‑κB signalling. CTSB constitutes a potential therapeutic target for the treatment of DOX‑induced cardiotoxicity.