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Effect of Smad3 knockout on doxorubicin cardiotoxity

ABSTRACT: Effect of Smad3 knockout on doxorubicin cardiotoxity

PROVIDER: PRJNA851761 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19783667_1.fastq.gz	Fastqsanger.gz
	SRR19783667_2.fastq.gz	Fastqsanger.gz
	SRR19783668_1.fastq.gz	Fastqsanger.gz
	SRR19783668_2.fastq.gz	Fastqsanger.gz
	SRR19783669_1.fastq.gz	Fastqsanger.gz

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Effect of Smad3 knockout on doxorubicin cardiotoxity

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Project description:Doxorubicin as a commonly used anthracycline has become the cornerstone of chemotherapy in a wide range of cancers owing to its high efficacy. However, clinical applications of doxorubicin are limited mainly due to its toxic effects on myocardium but the pathogenic mechanism of doxorubicin-induced cardiomyopathy are poorly understood. ADAM17 is known as tumor necrosis factor α converting enzyme (TACE), and the cleavage of TNF-α by ADAM17 is a prerequisite for pro-inflammatory TNF-α activity, which raises a possibility that inhibition of ADAM17 may exert a beneficial effect on disease processes where TNF-α plays an essential role. Our previous research has shown that cardiomyocyte specific knockout of ADAM17 improves diabetic cardiomyopathy by modulating cardiomyocyte apoptosis. However, the relationship between ADAM17 and doxorubicin-induced cardiomyopathy is unclear.Through RNA sequencing analysis, we observed significant changes in the TNF signaling pathway genes in the heart tissue of mice with or without cardiomyocyte ADAM17 knockout.

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