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Signaling response to personalized exercise therapy in skeletal muscle from heart failure patients with reduced ejection fraction.

ABSTRACT: Signaling response to personalized exercise therapy in skeletal muscle from heart failure patients with reduced ejection fraction.

PROVIDER: PRJNA556163 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9734000.fastq.gz	Fastqsanger.gz
	SRR9734001.fastq.gz	Fastqsanger.gz
	SRR9734002.fastq.gz	Fastqsanger.gz
	SRR9734003.fastq.gz	Fastqsanger.gz
	SRR9734004.fastq.gz	Fastqsanger.gz

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Signaling response to personalized exercise therapy in skeletal muscle from heart failure patients with reduced ejection fraction.

Project description:In chronic heart failure (CHF), functional and metabolic alterations are detected not only in cardiac muscle but also in skeletal muscle tissue. The molecular mechanisms responsible for muscle dysfunction in patients with CHF remain unknown as well as the biological processes responsible for the positive effect of physical exercise training. In this work, using the results of transcriptome sequencing (3' mRNA-Seq), authors identify the molecular mechanisms responsible for reducing muscle dysfunctions in patients with CHF undergoing a personalized program of physical rehabilitation. 3 patients with CHF were enrolled in the study, biopsies of gastrocnemius muscle were taken before and after 12 weeks of individual training program (intensity was determined at 90% of lactate inflection point). Analysis of RNA-Seq data shows the strong upregulation of pathways that control skeletal muscle cell differentiation, muscle contraction, recovery of membrane potential.

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Exercise Training Ameliorates Myocardial Phenotypes in Heart Failure with Preserved Ejection Fraction by Changing N6-methyladenosine Modification in Mice Mode

Project description:Heart failure with preserved ejection fraction (HFpEF) shows complicated and not clearly defined etiology and pathogenesis. Although no pharmacotherapeutics have improved the survival rate in HFpEF, exercise training has become an efficient intervention to improve functional outcomes. Here, we investigated N6-methyladenosine (m6A) RNA methylation modification in a “two-hit” mouse model with HFpEF and HFpEF with exercise (HFpEF + EXT). The manner of m6A in HFpEF and HFpEF + EXT hearts were explored via m6A-specific methylated RNA immunoprecipitation followed by high-throughput and RNA sequencing methods. A total amount of 3 992 novel m6A peaks were spotted in HFpEF+EXT, and 426 differently methylated sites, including 371 hypermethylated and 55 hypomethylated m6A sites, were singled out for further analysis (fold change >2, p < 0.05). Totally, m6A which is a significant alternation of epitranscriptomic processes, is a potentially meaningful therapeutic target.

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