4.7 Article

Genetic inhibition of serum glucocorticoid kinase 1 prevents obesity-related atrial fibrillation

期刊

JCI INSIGHT
卷 7, 期 19, 页码 -

出版社

AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/jci.insight.160885

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资金

  1. NIH [T32HL007604, 1R01HL092577]
  2. American Heart Association [20CDA35260081, 18IPA34170109]
  3. American Heart Association Strategically Focused Research Net- works [SFRN35120123]
  4. American Heart Association Strategically Focused Research Networks [18SFRN34110082]
  5. European Union [965286]

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This study validates the role of SGK1 in obesity-related atrial fibrillation using a mouse model. It demonstrates the impact of SGK1 on atrial electrophysiology, structural remodeling, inflammation, and sodium current in obesity-related AF.
Obesity is an important risk factor for atrial fibrillation (AF), but a better mechanistic understanding of obesity-related atrial fibrillation is required. Serum glucocorticoid kinase 1 (SGK1) is a kinase positioned within multiple obesity-related pathways, and prior work has shown a pathologic role of SGK1 signaling in ventricular arrhythmias. We validated a mouse model of obesity-related AF using wild-type mice fed a high-fat diet. RNA sequencing of atrial tissue demonstrated substantial differences in gene expression, with enrichment of multiple SGK1-related pathways, and we showed upregulated of SGK1 transcription, activation, and signaling in obese atria. Mice expressing a cardiac specific dominant-negative SGK1 were protected from obesity-related AF, through effects on atrial electrophysiology, action potential characteristics, structural remodeling, inflammation, and sodium current. Overall, this study demonstrates the promise of targeting SGK1 in a mouse model of obesity-related AF.

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