Introduction A large body of evidence recently highlighted the involvement of long non-coding RNAs (lncRNAs) in cardiovascular disease [1] and some dysregulated lncRNAs have been associated with diabetic cardiomyopathy [2–5]. Among them, a higher expression of the lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) has been observed in diabetic cardiomyopathy [6, 7]. However, a clear understanding of the molecular mechanisms leading to pathological regulation of lncRNAs in diabetic cardiomyopathy is still missing. Our prior work by Barbati et al. [8], established that, in the presence of high glucose, nitric oxide (NO) signaling derangement might alter the epigenetic landscape of cardiac cells, both in vitro and in vivo, via transcription factor CREM activation. Aim The present study is aimed at investigating the role of high glucose (HG) and NO pathway in the regulation of MALAT1 in the heart of mice after 6 months of prolonged hyperglycemia and in two cellular models of cardiomyocytes exposed to HG.
Original languageEnglish
Pages (from-to)259-262
Number of pages4
Publication statusPublished - 2018


  • Diabetes and Metabolism
  • Endocrinology
  • cyclic AMP responsive element modulator
  • glucose
  • metastasis associated lung adenocarcinoma transcript 1
  • nitric oxide


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