The Role of CCAAT/Enhancer-Binding Protein δ in Doxorubicin-Induced Cardiomyopathy

  • 溫 瑞慈

Student thesis: Master's Thesis


Heart failure (HF) is one of the leading causes of cardiovascular mortality and morbidity in the world In the treatment of cancer patients the chemical used in chemotherapy doxorubicin (DOX) can induce cardiomyopathy and HF DOX-induced HF in mice is a commonly used animal model to explore the mechanism and therapeutic tools During the process of cardiotoxicity and cardiomyopathy inflammation reactions occur C/EBP δ belongs to the CCAAT/enhancer binding protein (C/EBP) family of transcription factors and it is low in normal physiological conditions but will rapidly increase in number from certain external stimuli inducing signal transduction in the cell Some reports have suggested a role for C/EBP δ in the activation of the innate immune response and pro-inflammatory conditions It regulates the expression of in?ammatory genes Previous studies have shown that Cebpd deficiency could protect against lipopolysaccharide (LPS)-induced lung injury in vivo however few studies have examined the role of C/EBP δ on cardiomyocytes In our study intraperitoneal (i p ) injections DOX induced chronic inflammation reaction in mice heart Using cebpd knockout mice to test the role of C/EBP δ during the pathophysiologic course of HF We found that cebpd deficiency could reduce HF in the early stage while DOX treatment and improve the chance of survival In the future it may combine the inhibition of C/EBP δ with anti-inflammatory drugs to reduce the myocardial inflammatory responses in the chronic/acute HF patients It will ameliorate the heart injury in the early treatment and improve the more stable and healing opportunity
Date of Award2016 Jan 19
Original languageEnglish
SupervisorPing-Yen Liu (Supervisor)

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