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Canagliflozin combined with aerobic exercise protects against chronic heart failure in rats via regulating the retinol metabolism signaling pathway.

ABSTRACT: Canagliflozin combined with aerobic exercise protects against chronic heart failure in rats via regulating the retinol metabolism signaling pathway.

PROVIDER: PRJNA934087 | ENA |

REPOSITORIES: ENA

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	SRR23434116_1.fastq.gz	Fastqsanger.gz
	SRR23434116_2.fastq.gz	Fastqsanger.gz
	SRR23434117_1.fastq.gz	Fastqsanger.gz
	SRR23434117_2.fastq.gz	Fastqsanger.gz
	SRR23434118_1.fastq.gz	Fastqsanger.gz

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Canagliflozin combined with aerobic exercise protects against chronic heart failure in rats via regulating the retinol metabolism signaling pathway.

Project description:To determine the efficacy and potential protective mechanism of canagliflozin combined with aerobic exercise in treating chronic heart failure (CHF).During 10 days, isoproterenol (5 mg/kg/d) was injected into rats to create CHF models. The rats were then randomized into four groups and administered with saline, canagliflozin (3 mg/kg/d), aerobic exercise training, and canagliflozin combined with aerobic exercise training. Then, we performed gene expression profiling using the data obtained by RNA-seq in the Control, HF, LC and LC-AE groups.

2023-02-17 | GSE225149 | GEO

Canagliflozin combined with aerobic exercise protects against chronic heart failure in rats.

Project description:To determine the efficacy and potential protective mechanism of canagliflozin combined with aerobic exercise in treating chronic heart failure (CHF). Isoproterenol was injected into rats to create CHF models. The rats were then subsequently divided into saline, canagliflozin (3 mg/kg/d), aerobic exercise training, and canagliflozin combined with aerobic exercise training. Compared to the CHF group, the canagliflozin combined with the aerobic exercise group had superior ventricular remodeling and cardiac function. In rats treated with canagliflozin combined with aerobic exercise, the expression of cytochrome P450 (CYP) 4A3, CYP4A8, COL1A1, COL3A1, and FN1 was reduced, while the expression of CYP26B1, ALDH1A2, and CYP1A1 increased significantly. Additionally, canagliflozin combined with aerobic exercise decreased the phosphorylation of AKT and ERK1/2. Canagliflozin combined with aerobic exercise has a positive effect on the development of CHF via the regulation of retinol metabolism and the AKT/ERK signaling pathway.

| S-EPMC10910240 | biostudies-literature

Canagliflozin regulates ferroptosis to ameliorate heart failure in rats with preserved ejection fraction

Project description:Chronic heart failure (CHF), with whether reduced ejection fraction (HFrEF) or preserved ejection fraction (HFpEF), is the end-stage of various cardiovascular diseases and severely affects the patients’ lifespan. There has been no effective drugs to improve clinical outcomes for a long time. Sine the recent years, as a hypoglycemic drug, sodium-glucose cotransporter 2 inhibitor (SGLT2i) has aroused great attention due to it’s cardiovascular benefits. However, the underlying mechanisms remain unclear, particularly regarding ferroptosis, a newly defined mechanism of iron-dependent non-apoptotic cell death in heart failure (HF). Here, we discovered and demonstrated that ferroptosis was a key mechanism in rat model of high-salt diet-induced HF, characterized by iron overloading and lipid peroxidation, which was blocked by canagliflozin administration. These findings highlight that targeting ferroptosis serves as a cardioprotective strategy for HF prevention and canagliflozin might display cardiovascular benefits through ferroptosis mitigation.

2022-05-20 | PXD029031 | Pride

Combined aerobic and resistance exercise training alters the spatial transcriptome of skeletal muscle in young adults

Project description:Chronic exercise training substantially improves skeletal muscle function and performance. The repeated demands and stressors of each exercise bout drive coordinated molecular adaptations within multiple cell types in muscle tissue, leading to enhanced neuromuscular recruitment and contractile function, stem cell activation, myofiber hypertrophy, mitochondrial biogenesis, and angiogenesis, among others. To comprehensively profile molecular changes induced by combined resistance and endurance exercise training, we employed spatial transcriptomics coupled with immunofluorescence and computational approaches to resolve effects on myofiber and mononuclear cell populations in human muscle. By computationally identifying fast and slow myofibers using immunofluorescence data of spatially sequenced tissue sections, we identified fiber type-specific, exercise-induced gene expression changes that correlated with muscle functional improvements. Additionally, spatial transcriptome profiling and integration of human muscle single cell RNAseq data identified an exercise-induced shift in interstitial cell populations coincident with angiogenesis. Overall, these data provide a unique spatial molecular profiling resource for exploring muscle adaptations to exercise, and provide a pipeline and rationale for future studies in human muscle.

2025-07-10 | GSE270703 | GEO

Retinol Dehydrogenase 10 Reduction Mediated Retinol Metabolism Disorder Promotes Diabetic Cardiomyopathy

Project description:Diabetic cardiomyopathy (DCM) is a primary myocardial injury induced by diabetes mellitus (DM) with a complex pathogenesis. In this study, we identified disordered cardiac retinol metabolism in T2DM mice and patients characterized by retinol (vitamin A, Rol) overload, all-trans retinoic acid (atRA) deficiency and retinoic acid receptors (RARs) reduction, and demonstrated that both cardiac Rol overload and atRA deficiency promote DCM by supplementing T2DM mice with Rol or atRA. Mechanically, by constructing cardiomyocyte-specific conditional RDH10-knockout mice and overexpressing RDH10 in T2DM mice via adeno-associated virus, we verified that the reduction in cardiac retinol dehydrogenase 10 (RDH10) is the initiating factor for cardiac retinol metabolism disorder and its resulting DCM. Additionally, lipotoxicity and ferroptosis contribute to the effect of retinol metabolism disorder on DCM. Based on these results, we suggest that the reduction of cardiac RDH10 and its mediated disorder of cardiac retinol metabolism is a new mechanism underlying DCM.

2023-01-15 | GSE202418 | GEO

RNA-seq in gWAT from diabetic mice treated with canagliflozin

Project description:We found canagliflozin shows elimination of senescent cells from organs in age-related pathology mouse model including diabetes. To clarify detailed change by canagliflozin treatement, we conducted RNA-seq analysis in gonadal white adipose tissue(gWAT).

2024-04-06 | GSE252539 | GEO

The SGLT2 inhibitor canagliflozin suppresses growth and enhances prostate cancer response to radiotherapy

Project description:Radiotherapy (RT) is a non-invasive standard treatment for prostate cancer (PC). However, PC develops radio-resistance, highlighting a need for agents to improve RT response. Canagliflozin, an inhibitor of sodium-glucose co-transporter-2, is approved for use in diabetes and heart failure, but is also shown to inhibit PC growth. However, whether canagliflozin can improve RT response in PC remains unknown. Here, we show that well-tolerated doses of canagliflozin suppress proliferation and survival of androgen-sensitive and insensitive human PC cells and tumors and sensitize them to RT. Canagliflozin blocks mitochondrial respiration, promotes AMPK activity, inhibits the MAPK and mTOR-p70S6k/4EBP1 pathways, activates cell cycle checkpoints, and inhibits proliferation in part through HIF-1 suppression. Canagliflozin mediates transcriptional reprogramming of several metabolic and survival pathways known to be regulated by ETS and E2F family transcription factors. Genes downregulated by canagliflozin are associated with poor PC prognosis. This study lays the groundwork for clinical investigation of canagliflozin in PC prevention and treatment in combination with RT.

2023-09-10 | GSE239688 | GEO

Role of aerobic exercise in ameliorating NASH

Project description:To investigate the effect of aerobic exercise on liver injury in nonalcoholic steatohepatitis (NASH), we established a NASH model induced by atherosclerotic (Ath) diet and intervened with aerobic exercise training.

2023-01-11 | GSE217155 | GEO

Muscle Transcriptome Profile of Resistance Exercise is Augmented by Aerobic Exercise

Project description:10 male subjects performed ~45 min one-legged cycling and 4 x 7 maximal concentric-eccentric knee extensions for each leg 15 min later. Thus, one limb performed aerobic and resistance exercise (AE+RE), while the opposing leg did resistance exercise only (RE). Biopsies were obtained from m. vastus lateralis of each leg 3 h after the resistance exercise bout. Gene expression analysis was carried out on the Affymetrix HuGene-2.1-st platform.

2016-05-24 | GSE74194 | GEO

Resistance to aerobic exercise training causes metabolic dysfunction and reveals novel exercise-regulated signaling networks

Project description:Low aerobic exercise capacity is a risk factor for diabetes and strong predictor of mortality; yet some individuals are exercise resistant, and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease-risk, we used selective breeding for 15 generation to develop rat models of low- and high-aerobic response to training. Before exercise training, rats selected as low- and high-responders had similar exercise capacities. However, after 8-wks of treadmill training low-responders failed to improve their exercise capacity, while high-responders improved by 54%. Remarkably, low-responders to aerobic training exhibited pronounced metabolic dysfunction characterized by insulin resistance and increased adiposity, demonstrating that the exercise resistant phenotype segregates with disease risk. Low-responders had impaired exercise-induced angiogenes0is in muscle; however, mitochondrial capacity was intact and increased normally with exercise training, demonstrating that mitochondria are not limiting for aerobic adaptation or responsible for metabolic dysfunction in low-responders. Low-responders had increased stress/inflammatory signaling and altered TGFβ signaling, characterized by hyperphosphorylation of a novel exercise-regulated phosphorylation site on SMAD2. Using this powerful biological model system we have discovered key pathways for low exercise training response that may represent novel targets for the treatment of metabolic disease.

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