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Proline metabolic reprogramming modulates cardiac remodeling induced by pressure-overload in the heart [cardiac tissues]

ABSTRACT: Proline metabolic reprogramming modulates cardiac remodeling induced by pressure-overload in the heart [cardiac tissues]

PROVIDER: PRJNA1081822 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28150137_1.fastq.gz	Fastqsanger.gz
	SRR28150137_2.fastq.gz	Fastqsanger.gz
	SRR28150138_1.fastq.gz	Fastqsanger.gz
	SRR28150138_2.fastq.gz	Fastqsanger.gz
	SRR28150139_1.fastq.gz	Fastqsanger.gz

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Proline metabolic reprogramming modulates cardiac remodeling induced by pressure-overload in the heart [cardiac tissues]

Project description:Metabolic reprogramming is critical in the onset of pressure overload-induced cardiac remodeling. Our study reveals that proline dehydrogenase (PRODH), the key enzyme in proline metabolism, reprograms cardiomyocyte metabolism to protect against cardiac remodeling. We induced cardiac remodeling using transverse aortic constriction (TAC) in both cardiac-specific PRODH knockout and overexpression mice. Our results indicate that PRODH expression is suppressed post-TAC. Cardiac-specific PRODH knockout mice exhibited worsened cardiac dysfunction, while mice with PRODH overexpression demonstrated a protective effect. Additionally, we simulated cardiomyocyte hypertrophy in vitro using neonatal rat ventricular myocytes treated with phenylephrine. Through RNA sequencing, metabolomics, and metabolic flux analysis, we elucidated that PRODH overexpression in cardiomyocytes redirects proline catabolism to replenish tricarboxylic acid (TCA) cycle intermediates, enhance energy production, and restore glutathione redox balance. In summary, our findings suggest PRODH as a modulator of cardiac bioenergetics and redox homeostasis duing cardiac remodeling induced by pressure overload. This highlights the potential of PRODH as a therapeutic target for cardiac remodeling.

2025-02-28 | GSE260465 | GEO

Proline metabolic reprogramming modulates cardiac remodeling induced by pressure-overload in the heart [Cardiomyocyte]

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Proline metabolic reprogramming modulates cardiac remodeling induced by pressure-overload in the heart [Cardiomyocyte]

Project description:Proline metabolic reprogramming modulates cardiac remodeling induced by pressure-overload in the heart [Cardiomyocyte]

| PRJNA1081823 | ENA

Pressure overload cardiac hypertrophy

Project description:Expression profiling of hearts from FVB males subjected to cardiac pressure overload by transverse aortic constriction (TAC). TAC performed on 8-10 weeks month old males and females. Hearts examined 30 weeks after surgery. Keywords: ordered

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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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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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Differential gene expression in adrenal medulla after cardiac pressure overload

Project description:Transcriptom analysis of microdissect adrenal medulla after 8 weeks of cardiac pressure overload caused by transverse aortic constriction.

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Loss of Lin28a Attenuates Cardiac Hypertrophy Induced by Pressure Overload

Project description:Pathological cardiac hypertrophy is a major risk factor for the development of heart failure and sudden cardiac death, yet the molecular mechanism of cardiac hypertrophy is not fully understood. Recently, we found that the expression of Lin28a, a RNA-binding protein, was significantly upregulated during the early stages of cardiac hypertrophy. Interestingly, cardiac specific conditional deletion of Lin28a blunted pressure overload-induced cardiac hypertrophic responses. Given that Lin28a can bind to diverse mRNA to regulate their abundance and/or translation, we conducted RNA-seq to profile the cardiac transcriptome alteration without Lin28a under pressure overload. It showed that metabolic pathways, including glycolysis and biosynthetic pathway, were remarkedly affected. Thus, our study identifies Lin28a as a crucial regulator of cardiac hypertrophy via its role in metabolic programming.

2019-04-30 | GSE106897 | GEO

Transcription profiling of mouse IL-18 knockouts vs. wild types treated with pressure overload to examine cardiac hypertrophy

Project description:Pressure overload-induced cardiac hypertrophy was examined in IL-18 knockout and littermate control mice. Experiment Overall Design: 4 groups with RNA pooled from 5-6 per group. Role of IL-18 on gene expression in cardiac hypertrophy induced by pressure overload (transaortic constriction)

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Differential gene expression in stellate sympathetic ganglia after cardiac pressure overload

Project description:Transcriptom analysis of stellate sympathetic ganglia after 8 weeks of cardiac pressure overload caused by transverse aortic constriction.

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