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The SGLT2 Inhibitor Empagliflozin Enhances Metabolic Efficiency and Ameliorates Left Ventricular Hypertrophy in Myosin R403Q Mutant Hypertrophic Cardiomyopathy Mice

ABSTRACT: The SGLT2 Inhibitor Empagliflozin Enhances Metabolic Efficiency and Ameliorates Left Ventricular Hypertrophy in Myosin R403Q Mutant Hypertrophic Cardiomyopathy Mice

PROVIDER: PRJNA1124979 | ENA |

REPOSITORIES: ENA

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	SRR29442720_1.fastq.gz	Fastqsanger.gz
	SRR29442720_2.fastq.gz	Fastqsanger.gz
	SRR29442725_1.fastq.gz	Fastqsanger.gz
	SRR29442725_2.fastq.gz	Fastqsanger.gz

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The SGLT2 Inhibitor Empagliflozin Enhances Metabolic Efficiency and Ameliorates Left Ventricular Hypertrophy in Myosin R403Q Mutant Hypertrophic Cardiomyopathy Mice

Project description:Background: Hypertrophic cardiomyopathy (HCM) is a genetic cardiac disorder characterized by left ventricular hypertrophy (LVH), diastolic dysfunction, and impaired metabolic efficiency. This study investigates the therapeutic potential of the sodium-glucose cotransporter 2 inhibitor empagliflozin (EMPA) in ameliorating these pathological features in a mouse model carrying the myosin R403Q mutation. Methods: Male mice harboring the R403Q mutation were treated with EMPA for 16 weeks. We utilized multinuclear magnetic resonance spectroscopy (31P, 13C, 23Na MRS), alongside echocardiography, transcriptomic, proteomic, and phosphoproteomic profiling to assess metabolic, structural, and functional changes. Results: EMPA facilitated the coupling of glycolysis with glucose oxidation and normalized elevated intracellular sodium levels. Treatment resulted in a significant reduction in LVH and myocardial fibrosis as evidenced by echocardiography and histopathology. These structural improvements correlated with enhancements in mitochondrial ATP synthesis, fatty acid oxidation (FAO), and branched-chain amino acid (BCAA) catabolism. Furthermore, empagliflozin improved left ventricular diastolic function and contractile reserve, underscored by improved ATP production and reduced energy cost of contraction. Notably, these benefits were linked to downregulation of the mTOR signaling pathway and normalization of myocardial substrate metabolic fluxes. Conclusion: EMPA significantly mitigates structural and metabolic dysfunctions in a mouse model of HCM, underscoring its potential as a therapeutic agent for managing this condition. These findings suggest broader applicability of SGLT2 inhibitors in cardiovascular diseases, including those due to myocardial-specific mutations, warranting further clinical investigation.

2025-06-09 | GSE270093 | GEO

SGLT2 inhibitors and zebrafish

Project description:The CANVAS program revealed that the SGLT2 inhibitor canagliflozin increases the risk for lower-limb (minor) amputations in type 2 diabetics about a two-fold. On the contrary, the large RCTs with empagliflozin and dapagliflozin did not demonstrate a similar observation. Thus, a question arises whether the increased risk for minor amputations is associated only with canagliflozin or whether it is a class effect of SGLT2 inhibitors. Vascular disorders including defective angiogenesis are among the leading causes of lower-limb amputations. Therefore, here we examined the effects of empagliflozin, dapagliflozin, and canagliflozin on angiogenesis using zebrafish embryos and HUVECs.

2022-12-31 | GSE191046 | GEO

RNA-seq of cardiomyocytes exposed to glucose deprivation with or without empagliflozin treatment

Project description:Glucose-lowering drugs sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of serious heart failure events, regardless of diabetes status, but the underling mechanism of this cardioprotective benefit is unknown. Here, we performed RNA-seq screening in cardiomyocytes to determine the potential cardioprotective mechanism of empagliflozin (EMPA).

2022-12-12 | GSE200598 | GEO

transcriptional analysis of bulk monocytes isolated from patients post-bariatric surgery undergoing a standardized liquid mixed-meal test intended to provoque postprandial hypoglycemia, upon treatment with either placebo, anakinra or empagliflozin

Project description:Postprandial hypoglycemia is a disabling complication of bariatric surgery. So far, no therapy exists, and the underlying mechanisms remain unclear. Here, we hypothesized that glucose-induced IL-1β leads to an exaggerated insulin response in this condition. Therefore, we conducted a placebo controlled, randomized, double-blind, cross-over study with the SGLT2-inhibitor empagliflozin (Jardiance [10mg]) and the IL-1 receptor antagonist anakinra (Kineret [100mg]). Both drugs reduced postprandial insulin release and prevented hypoglycemia. Moreover, analysis of monocytes taken from this patient population ex-vivo revealed a hyper-reactive inflammatory state in these cells. Our study proposes a role for glucose-induced IL-1β in postprandial hypoglycemia after bariatric surgery and suggests that SGLT2-inhibitors and IL-1 antagonism may improve this condition.

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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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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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SGLT2 inhibitors and zebrafish

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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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Proteomic Analysis of the human Myocardium in non-hypertrophic control and hypertrophy patients

Project description:To explore the pathogenesis of myocardial hypertrophy, Proteomic Analysis was performed to identify the differentially expressed proteins in the human myocardial tissues of non-hypertrophic control and myocardial hypertrophy patients. We used echocardiography to detect the thickness of the ventricular septum in patients undergoing heart valve replacement surgery .The thickness of the ventricular septum over 11mm is defined as myocardial hypertrophy of patients, those less than or equal to 11mm were considered as non-hypertrophic controls. We collected a total of 6 cases of non-hypertrophic controls and 6 cases of myocardial hypertrophy patients' myocardial tissues, and Proteomic Analysis was performed by mass spectrometry.

2021-06-14 | PXD023778 | Pride

Single nucleus RNA-seq comparison of TYA018 HDAC6 inhibition and Empagliflozin SGLT2 inhibition to treat heart failure with preserved ejection fraction

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