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Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation [Ribo-seq]

ABSTRACT: Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation [Ribo-seq]

PROVIDER: PRJNA1011928 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25880419_1.fastq.gz	Fastqsanger.gz
	SRR25880419_2.fastq.gz	Fastqsanger.gz
	SRR25880420_1.fastq.gz	Fastqsanger.gz
	SRR25880420_2.fastq.gz	Fastqsanger.gz

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Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation [Ribo-seq]

Project description:Diabetes is associated with cardiovascular complications. microRNAs translocate into subcellular organelles to modify genes involved in diabetic cardiomyopathy. However, functional properties of subcellular Ago2, a core microRNA, remain elusive. We elucidated the function and mechanism of subcellular localized Ago2 on mouse models for diabetes mellitus and diabetic cardiomyopathy. Ago2 decreased in cardiomyocyte mitochondria in both models. Overexpression of mitochondrial Ago2 attenuated diabetes-induced cardiac dysfunction. Ago2 recruited TUFM, a mitochondria translation elongation factor, to activate translation of electron transport chain (ETC) subunits and decrease reactive oxygen species. Malonylation, a post-translational modification of Ago2, reduced the importing of Ago2 into mitochondria in diabetic cardiomyopathy. Ago2 malonylation was regulated by a cytoplasmic-localized short isoform of SIRT3 through a previously unknown demalonylase function. Our results reveal that the SIRT3–Ago2–CYTB axis links glucotoxicity to cardiac ETC imbalance, providing new mechanistic insights and the basis to develop mitochondria targeting therapies for diabetic cardiomyopathy.

2024-09-27 | GSE242185 | GEO

Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation II

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Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation [mRNA-seq]

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Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation [Ribosome-seq]

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Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation II

Project description:Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation II

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Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation [Ribosome-seq]

Project description:Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation [Ribosome-seq]

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Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation [mRNA-seq]

Project description:Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation [mRNA-seq]

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Cyclovirobuxine D protects against diabetic cardiomyopathy by activating Nrf2-mediated antioxidant responses.

Project description:Diabetic cardiomyopathy (DCM) is the principal cause of death in people with diabetes. However, there is currently no effective strategy to prevent the development of DCM. Although cyclovirobuxine D (CVB-D) has been widely used to treat multiple cardiovascular diseases, the possible beneficial effects of CVB-D on DCM remained unknown. The present aim was to explore the potential effects and underlying mechanisms of CVB-D on DCM. We explored the effects of CVB-D in DCM by using high fat high sucrose diet and streptozotocin-induced rat DCM model. Cardiac function and survival in rats with DCM were improved via the amelioration of oxidative damage after CVB-D treatment. Our data also demonstrated that pre-treatment with CVB-D exerted a remarkable cytoprotective effect against high glucose -or H2O2 -induced neonatal rat cardiomyocyte damage via the suppression of reactive oxygen species accumulation and restoration of mitochondrial membrane potential; this effect was associated with promotion of Nrf2 nuclear translocation and its downstream antioxidative stress signals (NQO-1, Prdx1). Overall, the present data has provided the first evidence that CVB-D has potential therapeutic in DCM, mainly by activation of the Nrf2 signalling pathway to suppress oxidative stress. Our findings also have positive implications on the novel promising clinical applications of CVB-D.

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Project description:Diabetic cardiomyopathy is a major health problem world wide. CTRP9 is a secreted glycoprotein, which is mainly expressed in endothelial cells of the heart. In this study, we investigated the impact of CTRP9 on diabetic cardiomyopathy induced by high fat diet feeding. While the lack of CTRP9 in knock-out mice aggravated the disease, AAV9 mediated cardiac CTRP9 overexpression ameliorated diastolic cardiac dysfunction under these conditions. Mechanistically, we found that CTRP9 is required for insulin dependent cardiac glucose uptake and metabolism and that it counteracts cardiac inflammation.

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2025-12-25 | GSE252044 | GEO

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