Dark Side of the Deep Heart
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Ischemic heart disease is the most common cause of death in Western countries.1 It is consequence of a reduced cardiac blood supply leading to a decrease in oxygen and nutrients fundamental for the proper functioning of the myocardium.1,2 The persistence of this condition induces fibrosis and scar deposition to replace the dead cardiac tissue.2 This replacement damages pumping function and thus predisposes to arrhythmias.3 Specific transcriptional programs finely regulate the cardiac remodeling.2 Deciphering the deep transcriptional changes during ischemic heart disease might shed light on potential targets for early diagnosis and new drug development.
See Article by Kaikkonen et al
Transcription permits to transform into RNA the coding and non-coding genetic information conserved into DNA. RNAs, in fact, are grouped into coding and non-coding transcripts (ncRNAs).4,5 The former, commonly known as mRNAs, are commonly translated into proteins, whereas the latter carry out mainly regulatory functions at transcriptional, post-transcriptional, and epigenetic levels.4,5 NcRNAs have been further classified, based on their length, into following types: small ncRNAs (<200 nucleotides) and long ncRNAs (lncRNAs; >200 nucleotides).4,5 microRNAs (miRNAs), transfer RNAs, piwi-interacting RNAs, and endogenous short interfering RNAs are examples of the first class.5 Instead, lncRNAs are generally categorized based on association to nearby protein-coding genes into following types: sense RNAs, antisense RNAs, intronic RNAs, intergenic RNAs, enhancer (eRNAs), and circular RNAs.4
RNA Polymerase II Pausing
All these RNAs are mostly transcribed by RNA polymerase II (Pol II), a multiprotein complex of 550 kDa localized into the nucleus of eukaryotic cells.6 Thanks to its prompt response to environmental signals, Pol II is able to immediately activate molecular mechanisms crucial for the …