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

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

PROVIDER: PRJNA762349 | ENA |

REPOSITORIES: ENA

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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

| PRJNA768421 | ENA

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.

2022-12-12 | GSE183932 | GEO

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

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

| PRJNA768422 | ENA

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.

2022-12-12 | GSE185265 | GEO

Targeting Immune-Fibroblast Crosstalk in Myocardial Infarction and Cardiac Fibrosis I

Project description:To define the cellular landscape of human myocardial infarction and heart failure, we performed Cellular Indexing of Transcriptomes and Epitomes by sequencing (CITE-seq) in 22 explanted human hearts from healthy donors, acute myocardial infarction (MI),and chronic ischemic and non-ischemic cardiomyopathy patients.

2024-07-01 | GSE217494 | GEO

myocardial infarction in Reg3beta knock-out mice

Project description:Affymetrix microarray analysis of molecular changes after myocardial infarction. Samples of heart tissue were analyzed after myocardial infarction from WT and reg3beta knock-out mice. Samples from scar tissue and samples adjacent to the scar were analyzed. In the experiment we primarily compared infarction zone of wild-type to infarction zone of knock-out animals, and remote zone of wild-type to remote zone of knock-outs.

2015-06-29 | E-MTAB-2561 | biostudies-arrayexpress

Cardiac organoid model of human myocardial infarction

Project description:Cardiac organoid model of human myocardial infarction

| PRJNA454314 | ENA

In Vivo Direct Reprogramming by AAV Improves Cardiac Function after Myocardial Infarction. [RNA-seq]

Project description:In Vivo Direct Reprogramming by AAV Improves Cardiac Function after Myocardial Infarction. [RNA-seq]

| PRJNA1033565 | ENA

Exacerbating role of angiopoietin-2 in cardiac hypoxia and inflammation after myocardial infarction

Project description:To unveil the role of Angiopoietin-2 in regulating vascular remodeling after myocardial infarction

2018-04-01 | GSE105223 | GEO

Trem2 Macrophage Promote Cardiac Repair in Myocardial Infarction via Efferocytosis and Carbohydrate Metabolism

Project description:We want to find that the TREM2 mechanism on the Macrophages in the myocardial infarction