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http://purl.uniprot.org/citations/31627188http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31627188http://www.w3.org/2000/01/rdf-schema#comment"

Background

Increased cardiac apoptosis is a hallmark of the elderly, which in turn increases the risk for developing cardiac disease. The overexpression of Omi/HtrA2 mRNA and protein contributes to apoptosis in the aged heart. Heat shock factor 1 (HSF1) is a transcription factor that binds to the promoter of Omi/HtrA2 in the aging myocardium. However, whether HSF1 participates in cardiomyocyte apoptosis via transcriptional regulation of Omi/HtrA2 remains unclear. The present study was designed to investigate whether HSF1 plays a role in Omi/HtrA2 transcriptional regulation and myocardial apoptosis.

Methods and results

Assessment of the hearts of mice of different ages was performed, which indicated a decrease in cardiac function reserve and an increase in mitochondrial apoptosis. Omi/HtrA2 overexpression in the elderly was negatively correlated with left ventricular function after exercise overload and positively correlated with myocardial Caspase-9 apoptosis. Chromatin immunoprecipitation (ChIP) of aging hearts and plasmid transfection/RNA interference of H9C2 cells revealed that enhancement of HSF1 expression promotes Omi/HtrA2 expression by inducing the promoter activity of Omi/HtrA2 while also increasing mitochondrial apoptosis by upregulating Omi/HtrA2 expression.

Conclusions

HSF1 acts as a transcriptional factor that induces Omi/HtrA2 expression and Caspase-9 apoptosis in aged cardiomyocytes, while also decreasing cardiac function reserve."xsd:string
http://purl.uniprot.org/citations/31627188http://purl.org/dc/terms/identifier"doi:10.18632/aging.102361"xsd:string
http://purl.uniprot.org/citations/31627188http://purl.uniprot.org/core/author"Liu H."xsd:string
http://purl.uniprot.org/citations/31627188http://purl.uniprot.org/core/author"Liu D."xsd:string
http://purl.uniprot.org/citations/31627188http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/31627188http://purl.uniprot.org/core/author"Ma X."xsd:string
http://purl.uniprot.org/citations/31627188http://purl.uniprot.org/core/author"Wu Y."xsd:string
http://purl.uniprot.org/citations/31627188http://purl.uniprot.org/core/author"Zhang S."xsd:string
http://purl.uniprot.org/citations/31627188http://purl.uniprot.org/core/author"Wei X."xsd:string
http://purl.uniprot.org/citations/31627188http://purl.uniprot.org/core/author"Wang W."xsd:string
http://purl.uniprot.org/citations/31627188http://purl.uniprot.org/core/author"Wu L."xsd:string
http://purl.uniprot.org/citations/31627188http://purl.uniprot.org/core/author"Yi M."xsd:string
http://purl.uniprot.org/citations/31627188http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31627188http://purl.uniprot.org/core/name"Aging (Albany NY)"xsd:string
http://purl.uniprot.org/citations/31627188http://purl.uniprot.org/core/pages"8982-8997"xsd:string
http://purl.uniprot.org/citations/31627188http://purl.uniprot.org/core/title"Heat shock factor 1-mediated transcription activation of Omi/HtrA2 induces myocardial mitochondrial apoptosis in the aging heart."xsd:string
http://purl.uniprot.org/citations/31627188http://purl.uniprot.org/core/volume"11"xsd:string
http://purl.uniprot.org/citations/31627188http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31627188
http://purl.uniprot.org/citations/31627188http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31627188
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http://purl.uniprot.org/uniprot/#_A0A075F6C2-mappedCitation-31627188http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31627188
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