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Empagliflozin in acute myocardial infarction reduces no-reflow and preserves cardiac function by preventing endothelial damage

ABSTRACT: Empagliflozin in acute myocardial infarction reduces no-reflow and preserves cardiac function by preventing endothelial damage

PROVIDER: PRJNA1077267 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27987727.fastq.gz	Fastqsanger.gz
	SRR27987728.fastq.gz	Fastqsanger.gz
	SRR27987729.fastq.gz	Fastqsanger.gz
	SRR27987730.fastq.gz	Fastqsanger.gz
	SRR27987731.fastq.gz	Fastqsanger.gz

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Empagliflozin in acute myocardial infarction reduces no-reflow and preserves cardiac function by preventing endothelial damage

Project description:Myocardial infarct size (IS) and now reflow are major determinants of prognosis and currently there are no effective treatments. We investigated the effects of empagliflozin on cardiac cell populations affected by myocardial ischemia reperfusion injury (IRI), and its cardioprotective potential in terms of IS and no-reflow.

2024-09-13 | GSE255933 | GEO

Empagliflozin in Acute Myocardial Infarction Reduces No-Reflow and Preserves Cardiac Function by Preventing Endothelial Damage.

Project description:Empagliflozin treatment before acute myocardial infarction mainly targets the endothelial cell transcriptome. Empagliflozin treatment before and after myocardial infarction decreased no reflow and microvascular injury, leading to reduced infiltration of inflammatory cells, reduced infarct size, and improved cardiac function in mice. In diabetic patients receiving empagliflozin after myocardial infarction, perfused boundary region, flow-mediated dilation, and global longitudinal strain were improved.

| S-EPMC11830260 | biostudies-literature

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Extracellular PKM2 Preserves Cardiomyocytes and Reduces Cardiac Fibrosis During Myocardial Infarction

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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

Empagliflozin alleviates atherosclerotic calcification by inhibiting osteogenic differentiation of vascular smooth muscle cells

Project description:SGLT-2 inhibitors, such as empagliflozin, have been shown to reduce the occurrence of cardiovascular events and delay the progression of atherosclerosis. However, its role in atherosclerotic calcification remains unclear. In this research, ApoE-/- mice were fed with western diet and empagliflozin was added to the drinking water for 24 weeks. Empagliflozin treatment significantly alleviated arterial calcification assessed by alizarin red and von kossa staining in aortic roots and reduced the lipid levels, while had little effect on body weight and blood glucose levels in ApoE-/- mice. In vitro studies, empagliflozin significantly inhibits calcification of primary vascular smooth muscle cells (VSMCs) and aortic rings induced by osteogenic media (OM) or inorganic phosphorus (Pi). RNA sequencing of VSMCs cultured in OM with or without empagliflozin showed that empagliflozin negatively regulated the osteogenic differentiation of VSMCs. And further studies confirmed that empagliflozin significantly inhibited osteogenic differentiation of VSMCs via qRT-PCR. Our study demonstrates that empagliflozin alleviates atherosclerotic calcification by inhibiting osteogenic differentiation of VSMCs, which addressed a critical need for the discovery of a drug-based therapeutic approach in the treatment of atherosclerotic calcification.

2023-11-22 | GSE243752 | GEO

TRIM13 affects cardiomyocyte injury and apoptosis through interacting with CD3D and regulating its ubiquitination in Myocardial Infarction

Project description:Myocardial infarction (MI) is a common cardiovascular disease with a high risk of sudden death. We aim to develop potential and more effective therapeutic strategies for treating and preventing MI.

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Bone marrow naïve B lymphocytes improve heart function after myocardial infarction [RNA-Seq]

Project description:We provided an mRNA-seq analyses of mouse bone marrow revealing B cell development arrest in the bone marrow after MI, which was restored by treatment of empagliflozin (EMPA).

2022-10-10 | GSE193425 | GEO

Bone marrow naïve B lymphocytes improve heart function after myocardial infarction [scRNA-Seq]

Project description:We provided a single cell mRNA-seq analyses of mouse bone marrow revealing B cell development arrest in the bone marrow after MI, which was restored by treatment of empagliflozin (EMPA).

2022-10-10 | GSE193316 | GEO

RNA-expression analysis on smooth muscle cells of diabetic donors after empagliflozin treatment

Project description:Purpose: We report vascular effects of empagliflozin stimulation. Results: Gene set enrichment analysis of RNA-Seq showed negative regulation of vascular smooth muscle cell proliferation. Gene set overlapped by the vasoactive peptide apelin, being upregulated by empagliflozin treatment.

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