Silenced long non-coding RNA activated by DNA damage elevates microRNA-495-3p to suppress atherosclerotic plaque formation via reducing Krüppel-like factor 5

MicroRNA‐495‐3p diminishes doxorubicin‐induced cardiotoxicity through activating AKT

“…Lin et al 25 revealed that miR ‐ 495 ‐ 3p upregulation promoted cell proliferation and inhibited apoptosis of tumour necrosis factor‐alpha‐induced human nucleus pulposus cells. Consistently, miR ‐ 495 ‐ 3p elevation significantly suppressed oxidative stress, endothelial dysfunction and fibrosis in atherosclerotic mouse aortas 26 . The present study aims to investigate the role and molecular mechanisms of miR ‐ 495 ‐ 3p in Dox‐induced cardiotoxicity.…”

“…Consistently, miR ‐ 495 ‐ 3p elevation significantly suppressed oxidative stress, endothelial dysfunction and fibrosis in atherosclerotic mouse aortas. 26 The present study aims to investigate the role and molecular mechanisms of miR ‐ 495 ‐ 3p in Dox‐induced cardiotoxicity.…”

Expression and clinical significance of lncRNA NORAD in patients with gestational hypertension

“…Similarly, Dai et al [30] detected the increased expression of lncRNA in patients with pregnancy-induced hypertension (including gestational hypertension and preeclampsia) through RT-qPCR. Fu et al [21] found that inhibition of NORAD inhibited inflammation, oxidative stress, and lipid levels of the atherosclerotic aorta in mice. Exploring the clinical information of the participants further confirmed that the SBP and DBP of patients with gestational hypertension and preeclampsia were higher than those of healthy people, and the expression level of NORAD was positively correlated with SBP and DBP.…”

“…NORAD has been proven to inhibit cell senescence, apoptosis, and atherosclerosis [20]. Silencing NORAD has been verified by reducing KLF5 to inhibit the formation of atherosclerotic plaque [21]. It is known that high blood pressure is a key risk factor for atherosclerosis, which influences each other and acts as a cause and effect for each other.…”

Upregulated NORAD is implicated in apoptosis, inflammation, and oxidative stress in ulcerative colitis through the nuclear factor-κappaB signaling

“…Activated by DNA damage (NORAD), also termed as linc00657, is a highly conserved lncRNA necessary for genome stability [21]. It was reported that NORAD exerts a promoting effect on some inflammatory diseases, such as psoriasis [22] and atherosclerosis [23]. NORAD has been unmasked to be regulated in UC patient-derived serums [24].…”