2020
DOI: 10.1007/s11010-020-03887-4
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LncRNA TTTY15 knockdown alleviates H2O2-stimulated myocardial cell injury by regulating the miR-98-5p/CRP pathway

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Cited by 14 publications
(10 citation statements)
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“…TTTY15 is highly expressed in hypoxia-induced endothelial cell injury and interference with its expression attenuates hypoxia-induced endothelial cell injury [11] . TTTY15 is up-regulated in patients with acute myocardial infarction and hydrogen peroxide-induced myocardial cell injury and knockdown of its expression reduces hydrogen peroxide-induced cardiomyocyte injury [12] . Inhibition of TTTY15 expression reduces hypoxia-induced cardiomyocyte injury [13] .…”
Section: Resultsmentioning
confidence: 99%
“…TTTY15 is highly expressed in hypoxia-induced endothelial cell injury and interference with its expression attenuates hypoxia-induced endothelial cell injury [11] . TTTY15 is up-regulated in patients with acute myocardial infarction and hydrogen peroxide-induced myocardial cell injury and knockdown of its expression reduces hydrogen peroxide-induced cardiomyocyte injury [12] . Inhibition of TTTY15 expression reduces hypoxia-induced cardiomyocyte injury [13] .…”
Section: Resultsmentioning
confidence: 99%
“…Previous studies have shown that TTTY15 is implicated in the regulation of a series of physiological and pathological processes. For example, knocking down TTTY15 reduces H 2 O 2 -induced cardiomyocyte injury via modulating the miR-98-5p/CRP axis [ 29 ]; TTTY15 can promote hypoxia-induced vascular endothelial cell injury by down-regulating miR-186-5p [ 30 ]. Importantly, TTTY15 is also involved in regulating the proliferation, differentiation, apoptosis and other biological processes of cancer cells [ 9 , 11 , 31 ].…”
Section: Discussionmentioning
confidence: 99%
“…It has been demonstrated that TTTY15 plays an important role in regulating hypoxia-induced vascular endothelial cell injury [48]. Knockdown of long noncoding RNA TTTY15 helps protect cardiomyocytes in case of hypoxia-induced apoptosis and 10 BioMed Research International mitochondrial energy metabolism dysfunction via TTTY15/ let-7i-5p and TLR3/NF-κB pathways [49]; and TTTY15 knockdown also protects cardiomyocytes from hypoxiainduced injury by regulating the let-7b/MAPK6 axis [50] or by regulating the miR-98-5p/CRP pathway [51]. Moreover, the polymorphism of ARHGAP9 is associated with coronary artery spasm [38].…”
Section: Discussionmentioning
confidence: 99%