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Direct In Vivo Cardiac Reprogramming as a Novel Therapeutic Strategy for Chronic Myocardial Infarction [scRNA-Seq]

ABSTRACT: Direct In Vivo Cardiac Reprogramming as a Novel Therapeutic Strategy for Chronic Myocardial Infarction [scRNA-Seq]

PROVIDER: PRJNA768422 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16193800_1.fastq.gz	Fastqsanger.gz
	SRR16193800_2.fastq.gz	Fastqsanger.gz
	SRR16193801_1.fastq.gz	Fastqsanger.gz
	SRR16193801_2.fastq.gz	Fastqsanger.gz
	SRR16193799_1.fastq.gz	Fastqsanger.gz

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Direct In Vivo Cardiac Reprogramming as a Novel Therapeutic Strategy for Chronic Myocardial Infarction

Project description:Direct In Vivo Cardiac Reprogramming as a Novel Therapeutic Strategy for Chronic Myocardial Infarction

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Direct In Vivo Cardiac Reprogramming as a Novel Therapeutic Strategy for Chronic Myocardial Infarction [Array]

Project description:Heart failure (HF) is a leading cause of morbidity and mortality. As adult cardiomyocytes (CMs) have little regenerative capacity, after myocardial infarction (MI), resident cardiac fibroblasts (CFs) synthesize extracellular matrix to form scar tissues, resulting in myocardial remodeling and HF. Thus, both cardiac regeneration and fibrosis are therapeutic targets for chronic MI. We previously reported that fibroblasts were directly reprogrammed into induced CMs (iCMs) by overexpression of cardiogenic transcription factors in vitro and in vivo in acute MI. Here we show that in vivo cardiac reprogramming generated iCMs from resident CFs, improved cardiac function, and reversed fibrosis in chronic MI using a novel transgenic mouse system. Transcriptome analysis revealed that in vivo cardiac reprogramming altered the interstitial cell landscape, suppressed signs of fibrosis and inflammation, and activated the angiogenic program. Thus, in vivo cardiac reprogramming may be a promising approach for chronic HF.

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Direct In Vivo Cardiac Reprogramming as a Novel Therapeutic Strategy for Chronic Myocardial Infarction [scRNA-Seq]

Project description:Heart failure (HF) is a leading cause of morbidity and mortality. As adult cardiomyocytes (CMs) have little regenerative capacity, after myocardial infarction (MI), resident cardiac fibroblasts (CFs) synthesize extracellular matrix to form scar tissues, resulting in myocardial remodeling and HF. Thus, both cardiac regeneration and fibrosis are therapeutic targets for chronic MI. We previously reported that fibroblasts were directly reprogrammed into induced CMs (iCMs) by overexpression of cardiogenic transcription factors in vitro and in vivo in acute MI. Here we show that in vivo cardiac reprogramming generated iCMs from resident CFs, improved cardiac function, and reversed fibrosis in chronic MI using a novel transgenic mouse system. Single-cell transcriptome analysis revealed that cardiac reprogramming shifted matrix-producing CFs, matrifibrocytes, to a quiescent state and changed the interstitial cell landscape, suppressing fibrotic and inflammatory signatures and activating angiogenic program. Thus, in vivo cardiac reprogramming may be a promising approach for chronic HF.

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