Matches in SemOpenAlex for { <https://semopenalex.org/work/W4386501600> ?p ?o ?g. }
- W4386501600 endingPage "3177" @default.
- W4386501600 startingPage "3163" @default.
- W4386501600 abstract "Doxorubicin (DOX) is a potent chemotherapeutic agent used against several cancer types. However, due to its cardiotoxic adverse effects, the use of this drug may be also life-threatening. Although most cancer patients are elderly, they are poorly represented and evaluated in pre-clinical and clinical studies. Considering this, the present work aims to evaluate inflammation and oxidative stress as the main mechanisms of DOX-induced cardiotoxicity, in an innovative approach using an experimental model constituted of elderly animals treated with a clinically relevant human cumulative dose of DOX. Elderly (18-20 months) CD-1 male mice received biweekly DOX administrations, for 3 weeks, to reach a cumulative dose of 9.0 mg/kg. One week (1W) or two months (2 M) after the last DOX administration, the heart was collected to determine both drug's short and longer cardiac adverse effects. The obtained results showed that DOX causes cardiac histological damage and fibrosis at both time points. In the 1W-DOX group, the number of nuclear factor kappa B (NF-κB) p65 immunopositive cells increased and a trend toward increased NF-κB p65 expression was seen. An increase of inducible nitric oxide synthase (iNOS) and interleukin (IL)-33 and a trend toward increased IL-6 and B-cell lymphoma-2-associated X (Bax) expression were seen after DOX. In the same group, a decrease in IL-1β, p62, and microtubule-associated protein 1A/1B-light chain 3 (LC3)-I, p38 mitogen-activated protein kinase (MAPK) expression was observed. Contrariwise, the animals sacrificed 2 M after DOX showed a significant increase in glutathione peroxidase 1 and Bax expression with persistent cardiac damage and fibrosis, while carbonylated proteins, erythroid-2-related factor 2 (Nrf2), NF-κB p65, myeloperoxidase, LC3-I, and LC3-II expression decreased. In conclusion, our study demonstrated that in an elderly mouse population, DOX induces cardiac inflammation, autophagy, and apoptosis in the heart in the short term. When kept for a longer period, oxidative-stress-linked pathways remained altered, as well as autophagy markers and tissue damage after DOX treatment, emphasizing the need for continuous post-treatment cardiac monitoring." @default.
- W4386501600 created "2023-09-08" @default.
- W4386501600 creator A5000876704 @default.
- W4386501600 creator A5023468464 @default.
- W4386501600 creator A5026062012 @default.
- W4386501600 creator A5027756968 @default.
- W4386501600 creator A5028035540 @default.
- W4386501600 creator A5039909767 @default.
- W4386501600 creator A5055195431 @default.
- W4386501600 creator A5080549181 @default.
- W4386501600 creator A5084255529 @default.
- W4386501600 date "2023-09-07" @default.
- W4386501600 modified "2023-10-15" @default.
- W4386501600 title "The role of inflammation and antioxidant defenses in the cardiotoxicity of doxorubicin in elderly CD-1 male mice" @default.
- W4386501600 cites W1489931849 @default.
- W4386501600 cites W1490258901 @default.
- W4386501600 cites W1964007788 @default.
- W4386501600 cites W1966078661 @default.
- W4386501600 cites W1976329823 @default.
- W4386501600 cites W1979200514 @default.
- W4386501600 cites W1981345102 @default.
- W4386501600 cites W1984646045 @default.
- W4386501600 cites W1987593270 @default.
- W4386501600 cites W1989935568 @default.
- W4386501600 cites W2000536297 @default.
- W4386501600 cites W2009175704 @default.
- W4386501600 cites W2009797078 @default.
- W4386501600 cites W2022760931 @default.
- W4386501600 cites W2030768343 @default.
- W4386501600 cites W2040736415 @default.
- W4386501600 cites W2051092344 @default.
- W4386501600 cites W2066653136 @default.
- W4386501600 cites W2072001961 @default.
- W4386501600 cites W2076631018 @default.
- W4386501600 cites W2082072877 @default.
- W4386501600 cites W2083911670 @default.
- W4386501600 cites W2094001942 @default.
- W4386501600 cites W2103017013 @default.
- W4386501600 cites W2106434524 @default.
- W4386501600 cites W2121836743 @default.
- W4386501600 cites W2127173211 @default.
- W4386501600 cites W2139357020 @default.
- W4386501600 cites W2152124377 @default.
- W4386501600 cites W2160302801 @default.
- W4386501600 cites W2167229817 @default.
- W4386501600 cites W2170591186 @default.
- W4386501600 cites W2313427064 @default.
- W4386501600 cites W2360592203 @default.
- W4386501600 cites W2508734629 @default.
- W4386501600 cites W2550513796 @default.
- W4386501600 cites W2560560709 @default.
- W4386501600 cites W2586749137 @default.
- W4386501600 cites W2766261199 @default.
- W4386501600 cites W2778620777 @default.
- W4386501600 cites W2782896483 @default.
- W4386501600 cites W2783983996 @default.
- W4386501600 cites W2789502860 @default.
- W4386501600 cites W2800400752 @default.
- W4386501600 cites W2802071168 @default.
- W4386501600 cites W2883639155 @default.
- W4386501600 cites W2884081989 @default.
- W4386501600 cites W2914541837 @default.
- W4386501600 cites W2944553255 @default.
- W4386501600 cites W2963901310 @default.
- W4386501600 cites W2987095718 @default.
- W4386501600 cites W2991822795 @default.
- W4386501600 cites W2998529369 @default.
- W4386501600 cites W2999797487 @default.
- W4386501600 cites W3012256530 @default.
- W4386501600 cites W3092578533 @default.
- W4386501600 cites W3111769181 @default.
- W4386501600 cites W3165549244 @default.
- W4386501600 cites W3174419361 @default.
- W4386501600 cites W3191430706 @default.
- W4386501600 cites W3208623356 @default.
- W4386501600 cites W3209518115 @default.
- W4386501600 cites W3215113693 @default.
- W4386501600 cites W4200250025 @default.
- W4386501600 cites W4211206037 @default.
- W4386501600 cites W4221069626 @default.
- W4386501600 cites W4225098794 @default.
- W4386501600 cites W4284989404 @default.
- W4386501600 cites W4309845455 @default.
- W4386501600 cites W4324142686 @default.
- W4386501600 doi "https://doi.org/10.1007/s00204-023-03586-1" @default.
- W4386501600 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37676301" @default.
- W4386501600 hasPublicationYear "2023" @default.
- W4386501600 type Work @default.
- W4386501600 citedByCount "0" @default.
- W4386501600 crossrefType "journal-article" @default.
- W4386501600 hasAuthorship W4386501600A5000876704 @default.
- W4386501600 hasAuthorship W4386501600A5023468464 @default.
- W4386501600 hasAuthorship W4386501600A5026062012 @default.
- W4386501600 hasAuthorship W4386501600A5027756968 @default.
- W4386501600 hasAuthorship W4386501600A5028035540 @default.
- W4386501600 hasAuthorship W4386501600A5039909767 @default.
- W4386501600 hasAuthorship W4386501600A5055195431 @default.
- W4386501600 hasAuthorship W4386501600A5080549181 @default.