2019
DOI: 10.1002/jcb.29162
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Interfering with long chain noncoding RNA ANRIL expression reduces heart failure in rats with diabetes by inhibiting myocardial oxidative stress

Abstract: This study is performed to elucidate whether long‐chain noncoding RNA ANRIL has an effect on diabetes, and further explore the mechanism of ANRIL in diabetes. The rat model of diabetes was established via intraperitoneal injection of streptozotocin. The modeled rats were grouped into normal, diabetes, siRNA‐NC, and ANRIL siRNA groups. Besides, the expression of ANRIL, cardiac function, inflammatory factor levels, cardiomyocyte apoptosis, and levels of oxidative stress index were all determined. Upregulated ANR… Show more

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Cited by 23 publications
(10 citation statements)
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“…Down‐regulated lncRNA‐GASL1 in CHF regulated cardiomyocyte apoptosis 51 . Interfering of lncRNA ANRIL reduces heart failure in rats with diabetes by inhibiting myocardial oxidative stress 52 . Lnc‐NOS2P3, the pseudogene 3, localizes in the same chromosome 17 neighbouring iNOS (NOS2).…”
Section: Discussionmentioning
confidence: 99%
“…Down‐regulated lncRNA‐GASL1 in CHF regulated cardiomyocyte apoptosis 51 . Interfering of lncRNA ANRIL reduces heart failure in rats with diabetes by inhibiting myocardial oxidative stress 52 . Lnc‐NOS2P3, the pseudogene 3, localizes in the same chromosome 17 neighbouring iNOS (NOS2).…”
Section: Discussionmentioning
confidence: 99%
“…In a murine model, silencing the expression of ANRIL (antisense lncRNA in the INK4 locus) improved the maladaptive myocardial remodelling and reduced the expression of inflammatory factors in ischaemic myocardial tissue of diabetic rats, by inhibiting myocardial oxidative stress [86,87].…”
Section: Long Noncoding Rna and Hfmentioning
confidence: 99%
“…Although the direct impact of these variants in human tissue or animal models is difficult to discern, work with mutations of ANRIL in endothelial models have provided valuable insight. Specifically, upregulation of ANRIL has been associated with increased expression of inflammatory and oxidative markers in the vascular tissue such as IL-6, IL-8, NF-κB, TNF-a, iNOS, ICAM-1, VCAM-1, and COX-2 (130,131). These observations provide vital information about cellular mechanisms impacted by human disease-associated genetic risk factors without requiring the expense and time investment of creating, validating, and studying animal models.…”
Section: Modeling Of Human Genomic Discoveriesmentioning
confidence: 99%