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Sirtuin 5 levels are limiting in preserving cardiac function and suppressing fibrosis in response to pressure overload

ABSTRACT: Sirtuin 5 levels are limiting in preserving cardiac function and suppressing fibrosis in response to pressure overload

PROVIDER: PRJNA817514 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18369500_1.fastq.gz	Fastqsanger.gz
	SRR18369500_2.fastq.gz	Fastqsanger.gz
	SRR18369501_1.fastq.gz	Fastqsanger.gz
	SRR18369501_2.fastq.gz	Fastqsanger.gz
	SRR18369502_1.fastq.gz	Fastqsanger.gz

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Sirtuin 5 levels are limiting in preserving cardiac function and suppressing fibrosis in response to pressure overload

Project description:Heart failure (HF) is defined as an inability of the heart to pump blood sufficiently to meet the metabolic demands of the body. HF with reduced systolic function is characterized by cardiac hypertrophy, ventricular fibrosis and remodeling, and decreased cardiac contractility, leading to cardiac functional impairment and death. Transverse aortic constriction (TAC) is a well-established model for inducing hypertrophy and HF in rodents. Mice globally deficient in sirtuin 5 (SIRT5), a NAD+-dependent deacylase, are hypersensitive to cardiac stress and display increased mortality after TAC. Prior studies assessing SIRT5 functions in the heart have all employed loss-of-function approaches. In this study, we generated SIRT5 overexpressing (SIRT5OE) mice, and evaluated their response to chronic pressure overload using TAC. Compared to littermate controls, SIRT5OE mice were protected against adverse functional consequences of TAC, left ventricular dilation, and impaired ejection fraction. Transcriptomic analyses revealed that SIRT5 suppresses key HF sequelae, including the metabolic switch from fatty acid oxidation to glycolysis, immune activation, and fibrotic signaling pathways. We conclude that SIRT5 is a limiting factor in the preservation of cardiac function in response to experimental pressure overload.

2022-03-23 | GSE198926 | GEO

Sirtuin 5 levels are limiting in preserving cardiac function and suppressing fibrosis in response to pressure overload

Project description:Heart failure (HF) is the inability of the heart to pump blood sufficiently to meet the metabolic demands of the body. HF with reduced systolic function is characterized by cardiac hypertrophy, ventricular fibrosis and remodeling, and decreased cardiac contractility, leading to cardiac functional impairment and death. Transverse aortic constriction (TAC) is a well-established model for inducing hypertrophy and HF in rodents. Mice globally deficient in sirtuin 5 (SIRT5), a NAD+-dependent deacylase, are hypersensitive to cardiac stress and display increased mortality after TAC. Prior studies assessing SIRT5 functions in the heart have all employed loss-of-function approaches. In this study, we generated SIRT5 overexpressing (SIRT5OE) mice, and evaluated their response to chronic pressure overload using TAC. Compared to littermate controls, SIRT5OE mice were protected against adverse functional consequences of TAC, left ventricular dilation and impaired ejection fraction. Transcriptomic analysis revealed that SIRT5 suppresses key HF sequelae, including the metabolic switch from fatty acid oxidation to glycolysis, immune activation, and fibrotic signaling pathways. We conclude that SIRT5 is a limiting factor in the preservation of cardiac function in response to experimental pressure overload.

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Pressure-Overload Induced Cardiac Hypertrophy

Project description:Aortic banding is an excellent model system to evaluate the process of development of left ventricular hypertrophy in response to hemodynamic stress. The Affymetrix GeneChip MgU74Av1 was used to analyze expression profiles of mice at different time points after surgical intervention for pressure-overload induced hypertrophy. More information about this model may be obtained at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/band_home.html Keywords = Pressure overload, cardiac hypertrophy Keywords: time-course

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Myocardial gene expression in response to pressure overload

Project description:Myocardial deletion of klf4 sensitizes mouse to pressure overload. In order to gain a better understanding of molecular mechanisms of such alterations, we profiled gene expression before and after 3-day of pressure overload (induced by transverse aortic constriction -TAC) in the hearts from MHC-cre (Cre) control and MHC-cre-klf4-deficient (KO) mice. 10wk old male mice was subjected to transverse aortic constriction (TAC) to induce pressure overload or sham operation as control group. After 3 days, heart was removed and total RNA was extracted from apex and subjected for array analysis. Four animals in each group.

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Pressure overload cardiac hypertrophy

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Myocardial gene expression in response to pressure overload

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Transcription profiling of mouse model of pressure overload

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Project description:Pressure overload-induced cardiac hypertrophy was examined in IL-18 knockout and littermate control mice. Keywords: genetic modification / disease model

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