Matches in SemOpenAlex for { <https://semopenalex.org/work/W4377564259> ?p ?o ?g. }
- W4377564259 abstract "Anthracyclines such as doxorubicin (Dox) are effective chemotherapeutic agents; however, their use is hampered by subsequent cardiotoxicity risk. Our understanding of cardiomyocyte protective pathways activated following anthracycline-induced cardiotoxicity (AIC) remains incomplete. Insulin-like growth factor binding protein (IGFBP) 3 (Igfbp-3), the most abundant IGFBP family member in the circulation, is associated with effects on the metabolism, proliferation, and survival of various cells. Whereas Igfbp-3 is induced by Dox in the heart, its role in AIC is ill-defined. We investigated molecular mechanisms as well as systems-level transcriptomic consequences of manipulating Igfbp-3 in AIC using neonatal rat ventricular myocytes and human-induced pluripotent stem cell-derived cardiomyocytes. Our findings reveal that Dox induces the nuclear enrichment of Igfbp-3 in cardiomyocytes. Furthermore, Igfbp-3 reduces DNA damage, impedes topoisomerase IIβ expression (Top2β) which forms Top2β-Dox-DNA cleavage complex leading to DNA double-strand breaks (DSB), alleviates detyrosinated microtubule accumulation—a hallmark of increased cardiomyocyte stiffness and heart failure—and favorably affects contractility following Dox treatment. These results indicate that Igfbp-3 is induced by cardiomyocytes in an effort to mitigate AIC." @default.
- W4377564259 created "2023-05-24" @default.
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- W4377564259 date "2023-05-23" @default.
- W4377564259 modified "2023-09-29" @default.
- W4377564259 title "Integrative transcriptomics and cell systems analyses reveal protective pathways controlled by Igfbp‐3 in anthracycline‐induced cardiotoxicity" @default.
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- W4377564259 doi "https://doi.org/10.1096/fj.202201885rr" @default.
- W4377564259 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37219486" @default.
- W4377564259 hasPublicationYear "2023" @default.
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