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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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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

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.

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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.

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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).

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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).

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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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CCN3 administration after surgically induced myocardial infarction

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Project description:Analysis of peripheral blood specimens from patients with acute myocardial infarction (AMI). Results provide insight into molecular mechanisms associated with AMI.

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RNA seq analysis of human macrophages after treatment of glimepiride versus empagliflozin.

Project description:Purpose: The goal of this study is to compare NGS-derived macrophage transcriptome profiling (RNA-seq) between diabetic patients treated with glimepiride versus empagliflozin. Methods: Macrophage mRNA profiles of 7 patients treated with either glimepiride or empagliflozin were generated by deep sequencing using Illumina HiSeq 4000 system. The sequence reads that passed quality filters were analyzed at the transcript isoform level using CLC Genomics Workbench v.9.0.1 software (CLC Bio, Cambridge, USA). Conclusion: A total of 64 genes were differentially expressed in the glimepiride treated patients compared to those of the empagliflozin treated patients, with 47 genes increased and 17 genes decreased in the glimepiride group. Most of these genes were related to immune-related receptor signaling pathway.

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